How to perform an optimal saline bubble contrast echo study

Saline bubble contrast echo studies, sometimes called agitated saline studies, are used in echocardiography to test for the presence of a right-to-left shunt at the intracardiac or intrapulmonary level. But what's the best way to perform such a study? Here are some tips.

Saline bubble contrast echo study showing PFO (right atrium opacified,

and red arrow shows small number of bubbles crossing into left atrium)

In order to perform a saline bubble contrast echo study, we need to create macroscopic bubbles in a syringe of saline. To prepare this, we draw up 8 mL of sterile normal saline in a 10 mL syringe, plus 0.5 mL of room air. We also add 1 mL of the patient's blood to the mixture, which helps create smaller bubbles and thereby provides better opacification of the right atrium.

To create the macroscopic bubbles, the saline/air/blood mixture needs to be agitated, and this is effectively done using a second 10 mL syringe attached to the first syringe via a 3-way tap. Always use Luer-lock syringes to avoid one of the syringes becoming detached and spraying everyone with the mixture!

By agitating the saline/air/blood mixture back and forth between the two syringes, a suspension of macroscopic bubbles is created. This is the saline bubble contrast.

This contrast is then immediately injected as an intravenous bolus via a cannula in an antecubital vein (ideally at least 20-gauge), while the echo images are obtained. A saline bubble contrast procedure can be performed during transthoracic or transesophageal echo. An echo window should be chosen that gives a clear view of both atria and the interatrial septum.

If the patient is suspected to have a persistent left-sided superior vena cava, then both left and right arm injections should be used to help clarify the diagnosis - in PLSVC, a right arm injection will opacify the right atrium normally, but a left arm injection will opacify the coronary sinus before the right atrium.

As soon as the bolus of saline bubble contrast is seen to arrive in the right atrium, the patient should perform a manoeuvre to transiently raise right atrial pressure - if there is a right-to-left shunt, this will increase the likelihood of bubbles crossing into the left atrium, and therefore this increases the sensitivity of the study. Suitable manoeuvres include:

• coughing
• release of a Valsalva manoeuvre

The timing with which bubbles appear in the left atrium (if at all) should be noted. With an intracardiac shunt (e.g. a patent foramen ovale), bubbles will normally appear in the left atrium within three cardiac cycles of the right atrium opacifying. However with an intrapulmonary shunt, there will normally be at least five cardiac cycles before bubbles appear in the left atrium.

Useful guidelines on the performance of contrast echo (including both saline bubble contrast and also transpulmonary ultrasound contrast agents) have been published by the ASE and can be found by clicking here.

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Ten key facts about atrial septal defect

Atrial septal defect (ASD), in which there is a communication in the interatrial septum allowing flow between left and right atria, is one of the commonest congenital heart problems. Here are Ten Key Facts about ASD that you should be aware of in your cardiology clinic:

TEE with colour Doppler, showing a secundum ASD

1. The commonest form of ASD is the secundum type, which accounts for 80% of cases. A secundum ASD is located in the region of the fossa ovalis.
2. Primum ASD accounts for 15% of cases, and is located near the crux of the heart, often involving the mitral and/or tricuspid valves.
3. Primum ASD is the most common congential heart defect seen in patients with Down syndrome.
4. Other types of ASD include superior sinus venosus defect, inferior sinus venosus defect, and unroofed coronary sinus.
5. An ASD most commonly causes left-to-right atrial shunting and consequent volume overload of the right heart.
6. ASD is commonly asymptomatic until adulthood.
7. Clinical examination findings in ASD include fixed splitting of the second heart sound, and a pulmonary flow murmur in systole.
8. ASDs can be closed percutaneously or by surgical repair. For secundum ASDs, percutaneous device closure is the preferred method of closure, and is technically feasible in around 80% of cases. 
9. The development of pulmonary hypertension due to pulmonary overcirculation can, eventually, lead to reversal of the interatrial shunt to right-to-left, and therefore cause cyanosis. This is known as Eisenmenger physiology, and is relatively rare (<5% of cases).
10. ASD closure should be avoided if a patient has developed Eisenmenger pathology.

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Spodick's sign: Downsloping TP segment in pericarditis

There are lots of eponymous signs in ECG interpretation (Wellens, Mobitz, Wenckebach and so on), so it's always interesting to discover a new one. That's what happened to me this week when I stumbled across Spodick's sign, which is used in the ECG diagnosis of pericarditis.

Spodick's sign refers to concave JT-segment elevation followed by a slight downsloping of the TP-segment. This slight downsloping in highlighted by the red arrows in the figure below, which shows ECG lead II in a patient with acute pericarditis.

Spodick's sign: Downsloping of the TP segment

Spodick's sign is reported to be present in around 80% of cases of acute pericarditis, although the reliability of the sign as a diagnostic indicator has been questioned by some.

Spodick's sign is named for David H. Spodick, who is Professor of Medicine Emeritus at the University of Massachusetts Medical School. You can read some of his publications on the ECG pericarditis here and here.

Have you spotted Spodick's sign on an ECG in pericarditis? Have you found it diagnostically helpful? Why not post a comment below?

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16 eponymous signs in aortic regurgitation

Aortic regurgitation has more eponymous signs than any other clinical condition. Here are sixteen of them to look out for next time you're in the cardiology clinic.

Colour M-mode study showing aortic regurgitation

Becker's sign
Prominent pulsation of the retinal arteries

Corrigan's sign
Prominent pulsation of the carotid arteries

De Musset's sign
Head nodding in synchrony with the pulse

Duroziez's sign
Systolic and diastolic murmurs heard over the femoral artery while the vessel is being partially compressed by the stethoscope

Gerhardt's sign
Pulsation of the spleen

Hill's sign
A higher systolic blood pressure (>20 mmHg) in the legs than in the arms

Landolfi's sign
Constriction/dilatation of the pupil in synchrony with the pulse

Lighthouse sign
Flushing of the forehead in synchrony with the pulse

Lincoln sign
Prominent (excessive) pulsation of the popliteal artery

Mayne's sign
A drop in diastolic blood pressure of >15 mmHg after raising the arm above the head

Mueller's sign
Pulsation of the uvula

Quincke's sign
Prominent pulsation of the capillaries in the nail beds

Rosenbach's sign
Pulsation of the liver

Sherman sign
Prominent pulsation of the dorsalis pedis artery

Traube's sign
A double sound auscultated over the femoral artery during distal compression

Watson's water hammer pulse
A collapsing pulse palpated at the patient's forearm

If you know of any others, you can add them to the Comment section below this blog.

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Echo assessment of LV diastolic function

Assessing left ventricular diastolic function can get complicated. However, things were made a bit easier recently with the publication of some new joint ASE/EACVI guidelines on the echo evaluation of LV diastolic function. The guidelines are detailed (they're almost 40 pages long), but the principal take home message can be summarized as follows:

Echo diagnosis of LV diastolic dysfunction

The guidelines recommend measuring four key parameters to assess LV diastolic function:

Annular e' velocity

An abnormal e' velocity is indicated by a septal e' <7 cm/s, or a lateral e' <10 cm/s.

Average E/e' ratio

The authors recommend that an average E/e' ratio is used (rather than separate septal and lateral E/e' ratios), and that the average E/e' ratio is considered to be abnormal if it is >14. If an average can't be calculated, then a lateral E/e' >13, or a septal E/e' >15, is considered to be abnormal.

Left atrial volume index

The left atrial maximum volume index is abnormal if it is >34 mL/m2.

Peak tricuspid regurgitation velocity

This is abnormal if peak TR velocity is >2.8 m/s.

Judging whether LV diastolic function is normal or abnormal depends upon how many of the measured parameters are abnormal:

• If more than 50% of the measured variables are abnormal, then LV diastolic function is abnormal
• If less than 50% of the measured variables are abnormal, then LV diastolic function is normal
• If 50% of the measured variables are abnormal, then LV diastolic function is indeterminate

This method of using the majority of available parameters to make an overall judgement about LV diastolic function is useful, as it allows a conclusion to be made about diastolic function even if all four parameters aren't available.

The guidelines can be found by clicking here, and are well worth reading. As well as giving overall advice about the echo assessment of LV diastolic function, they also contain guidance on assessing diastolic function in specific situations (such as atrial fibrillation and hypertrophic cardiomyopathy).

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Making sense of S2, the second heart sound

In our blog a few days ago, we looked at the first heart sound and how it varies with different clinical conditions. In today's blog, we're going to take a look at S2, the second heart sound.

The second heart sound is made up of two components:

• A2, caused by aortic valve closure
• P2, caused by pulmonary valve closure.

In expiration, the A2 and P2 components are virtually indistinguishable (in adults) and are essentially heard as a single sound. However in inspiration, the increase in venous return to the right heart slightly delays right ventricular emptying, which in turn slightly delays P2. Thus in inspiration we hear normal physiological splitting of the second heart sound, with P2 occurring just after A2.

This physiological splitting of the second heart sound gets wider (and therefore easier to auscultate) if P2 occurs late - this happens in right bundle branch block (because of the later contraction of the right ventricle), and also in pulmonary stenosis (due to greater impedance to right ventricular emptying). As you might expect, splitting of the second heart sound also gets wider if A2 occurs early - this is seen with mitral regurgitation, and also in ventricular septal defect, because left ventricular emptying occurs more quickly.

The splitting of the second heart sound becomes reversed (i.e. A2 occurs after P2) if emptying of the left ventricle is delayed - as occurs in left bundle branch block or aortic stenosis. When reversed splitting occurs, it's easiest to hear in expiration.

Transesophageal echo showing a secundum ASD

Fixed splitting of the second heart sound occurs in the presence of an atrial septal defect. In this situation, pressure changes with respiration affect the right and left atria equally, and so we no longer see the delay in P2 that normally occurs during inspiration.

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Ten key facts about S1, the first heart sound

When we auscultate the heart, we normally hear the first (S1) and second (S2) heart sounds. Here are ten key facts about the first heart sound to be aware of when you're examining patients.

Factors that affect the intensity of the first heart sound (S1)

1. The first heart sound (S1) results from mitral and tricuspid valve closure.
2. Although S1 has two separate components (the mitral component and the tricuspid component), they occur so close together that they're normally heard as a single sound.
3. If the patient's circulation is hyperdynamic, S1 will be louder than usual.
4. Conversely, S1 will be quiet if the patient has a low cardiac output.
5. S1 is louder than normal in Wolff-Parkinson-White syndrome. Why? Because the short PR interval in WPW syndrome means that the mitral leaflets are still widely separated at the start of systole.
6. Conversely, S1 will be quiet in the PR interval is long. This is because the mitral valve leaflets have already started to close by the time that systole begins.
7. S1 is louder than normal in mitral stenosis, for the same reason as with a short PR interval - in mitral stenosis, the slow exit of blood from the left atrium through the narrowed mitral valve means that the ventricle is still filling with blood, and thus the mitral leaflets are still widely separated, at the start of systole.
8. In mitral stenosis, S1 can be so loud that it can be palpated at the apex. This is described as a 'tapping' apex beat, the palpable first heart sound in mitral stenosis.
9. S1 is quieter than normal in mitral regurgitation.
10. An S1 of variable intensity is heard with atrial fibrillation, ectopic beats and complete heart block.

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