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Ascending Aortic Dissection |ASD

Here we examine two additional topics. These are not covered as the main topics related to focused cardiac ultrasound (FoCUS) examination. However they are part of the Objective Structured Clinical Examination Content for Anesthesiology. Aortic dissection is a catastrophic event that must be recognized early and that we actively participate in management either in the OR or our ICUs. Atrial septal defects on the other hand are the most common congenital heart defect associated with physiologic and ultimately in maladaptive changes in the long run that we must recognize. 

Aortic Dissection
Gradient

Aortic Dissection

Aortic dissection often presents acutely as a catastrophic illness with acute hemodynamic compromise. Early and accurate diagnosis and treatment are crucial for survival. Death from aortic dissection is related to its location. A proximal tear  (Stanford Type A) originates near the sinotubular junction (65% of cases) can compromise proximal as well as distal structures. This can lead to pericardial effusion precipitating cardiac tamponade; or lead to severe aortic regurgitation or obstruction of the coronary artery ostia leading to myocardial infarction. It could also lead to end-organ failure due to abdominal aortic branch vessel obstruction. A more distal origin (Stanford Type B) involves left subclavian artery (30% of cases) and extends into the descending thoraci and thoracoabdominal aorta. 

Dissection_edited.jpg

  Stanford Type A  

Stanford Type B

Classification of Aortic Dissection. The triangle marks the origin of the dissection

Patients with an acute aortic dissection presenting with hypotension typically imply cardiac tamponade, aortic rupture, or heart failure associated with severe aortic regurgitation. Clinically, sudden onset of back or chest pain associated with pulse deficits or aortic regurgitation should trigger a consideration for aortic dissection.

Surface echocardiography is not the first choice for diagnosis since it has a much lower sensitivity and specificity of diagnosis as compared to trans esophageal echocardiography or multidetector CT. However the presence of a pericardial effusion and or acute aortic insufficiency should alert the clinician that the patient is actually presenting with an aortic dissection. To review that content click on the following links.

On the following clips we can appreciate a dilated ascending aorta. We can also appreciate a dissection flap that involves the aortic valve. An aortic root diameter greater than 4cm is suggestive of Type A dissection. The aortic valve itself appears to have prolapsed implying severe aortic valve regurgitation. Image courtesy of The POCUS Atlas.

Multiple imaging modalities can be used to visualize dissection. These include CT angiography (this being the most common initial choice), MR angiography and TEE. TEE has a high sensitivity of 98% and specificity of 100%.  In the following TEE clips we can see a Stanford Type A dissection. The true (B) and false lumens (A, C) with the use of color flow doppler and an enlarged ascending aorta is seen. Within a few cm from the the sinotubular juction we can appreciate drop of.

Gradient

Atial Septal Defects (ASD)

ASDs are the most common congenital heart lesions seen in adults. They result from lack of tissue to completely septate the atria and are classified according to their location in the atrial septum.  The secundum ASD accounts for up to 3/4 of all cases and result from poor growth of the septum secundum. Primum ASD (1 in 5 cases) results from failure of the septum primum to fuse to the endocardial cushions and are almost always associated with anomalies of the atrioventricular valves. Sinus venosus (1 in 10 cases) result from an abnormality in the insertion of the superior or inferior vena cava. 

Patients present with right sided volume overload. And its diagnosis and evaluation involves demonstration of the presence, location, size, and direction of the shunt, as well as evaluation of any associated cardiac lesions and complications including RV volume overload, pulmonary hypertension, and arrhythmia. Surface echocardiography is the imaging study of choice for ASDs and a comprehensive study is needed to evaluate location as well as hemodynamic implications and thus out of the scope of focused cardiac ultrasound (FoCUS). Regardless,  the interatrial septum is often best visualized in the subcostal view in which the ultrasound beam is generally nearly perpendicular to the atrial septum and the apical 4 chamber view may not be relied upon due to the usual dropout artifact encountered on this view. 

Surface echo is usually diagnostic for secundum and primum ASDs when a complete examination (including multiple precordial windows) are performed. Clues to the presence of a secundum or primum defect include abrupt discontinuity or drop out of the interatrial septum. These also include hypermobility of the septum, particularly in association with an abrupt discontinuity, is also suggestive of secundum defect. TEE is superior to TTE for imaging the IAS and is often used when a definitive diagnosis is not made by TTE. 

On the following views we see a normal interatrial septum followed by an ASD on the apical 4 chamber view. Then a positive bubble study. The injection of agitated saline on a peripheral vein. There are bubbles present in the LV within 3 cardiac cycles after they appear on the right sided structures which implies an ASD is present. An ASD can also be seen directly on this modified bicaval view with the use of Color Flow Doppler and the presence of a left to right shunt indicated by the direction of flow. 

Atrial Septal Defects

References

1. Patil TA, Nierich A. Transesophageal echocardiography evaluation of the thoracic aorta. Ann Card Anaesth. 2016;19(Supplement):S44-S55. doi:10.4103/0971-9784.192623

2. Silvestry F E and all. Guidelines for the Echocardiographic Assessment of Atrial Septal Defect and Patent Foramen Ovale: From the American Society of Echocardiography and Society for Cardiac Angiography and Interventions. J Am Soc Echocardiogr 2015;28:910-58

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