Welcome to the Ultrasound Leadership Academy (ULA) summary blog series. This week, we discuss the basics of diastology. The ULA is essentially an online advanced ultrasound education experience put on by the team from Ultrasound Podcast which brings cutting edge learning to emergency medicine personnel through a variety of interactive platforms including video lectures, google hangouts with experts, simulation, live conferences and real time scanning with a pocket-sized ultrasound device known as a Vscan.
Over the next year I will be posting summaries of the key learning points from my experience. If you want to learn more about the program you can visit Ultrasound Leadership Academy or Ultrasound Podcast to see more from the hosts of this awesome program.
The elusive entity termed diastolic heart failure is something we always discuss in theory but often find it is quite difficulty to diagnose. Our major understanding of heart failure revolves around the idea of a pump that is failing and not providing enough forward flow. While the majority of patients presenting in heart failure will have systolic dysfunction, it is useful to grasp the idea of diastolic dysfunction, its pathophysiology, and how we can use ultrasound to assist with making this diagnosis rapidly and confidently. So the next time you see a patient presenting with shortness of breath who appears to have a normal EF on your bedside echo don't scratch off acute diastolic failure just yet, take a minute or two extra to look further.
The other term we frequently hear with regard to diastolic dysfunction is heart failure with preserved ejection fraction. In other words, their is adequate pump however the ventricle will demonstrate either impaired early diastolic relaxation (energy dependent process), increased stiffness (passive), or both. For example, acute myocardial ischemia can transiently lead to poor energy delivery to the myocardium and impaired diastolic relaxation while left ventricular hypertrophy and/or fibrosis will cause the LV walls to become stiffened. The end result of both of these processes is poor ventricular filling, which initially is accommodated for by increased filling pressures (increasing preload) but ultimately will lead to increasing demand on the myocardium and vascular congestion transmitted retrograde to the pulmonary and systemic veins (volume overload).
Now we have a patient whom we are concerned may have acute diastolic heart failure, let's briefly discuss the steps to make the diagnosis:
- Left atrium assessment
- Mitral inflow velocity
- Tissue doppler velocity at the septal annulus
Left atrium assessment
The simple way to assess for diastolic dysfunction, though subjective, is to look at the left atrium. Does it appear enlarged? This will give you an idea that there is some diastolic issue. A left atrium area of > 20 cm2 is very sensitive for diastolic dysfunction though is not as useful in the acute setting.
Mitral inflow velocity
Obtain an apical four chamber view with visualization of both the mitral and tricuspid valve. Using power doppler, place your gate just distal to the mitral valve (apical to the leaflets), directed inline with blood flow. You will be measuring the velocity of flow from the atrium to the ventricle here. Looking at the waveforms above, we see the E wave, which represents early passive atrial filling, and the A wave, which represents the atrial kick. Notice that diastolic dysfunction is not dichotomous but more of a spectrum of disease.
- Normal: You will observe the E wave > the A wave. This means that the heart is predominately filling passively from venous return and requires less from the atrial kick.
- Impaired relaxation: As relaxation of the LV becomes impaired, passive filling decreases and atrial kick is now generating higher velocity from increased pressures (E wave < A wave).
- Pseudo-normalization: Moving further along the spectrum of disease, initial compensatory mechanisms result in increased preload, increasing filling pressures, leading to the observed pseudo normalization of waveforms as seen above. The E wave again appears greater than the A wave (Refer back to pressure volume loop above as to why this is not a good compensatory mechanism).
- Restrictive: Preload continues to increase and filling pressures are now significantly elevated. Essentially the blood in dumping into the ventricle as soon as the mitral valve opens and the atrial kick can no longer contribute much. The E wave now appears >> the A wave.
Tissue doppler velocity at septal annulus
If you are seeing massive E waves with tiny A waves you are probably done, however often you may run into the pseudo-normal pattern and may want to gather some more information. Your next step will be to perform tissue doppler on the septal annulus.
- Change your scale to negative velocities (around 0 to -20 or -30).
- Turn down your overall image gain to avoid velocities that go out of your range.
- Obtain your apical view and place the power doppler gate at the septal annulus (where the mitral valve attaches to the septum). You will be measuring the speed at which the ventricle descends during early diastole.
In a normal ventricle, the speed should be > 8 cm/s, however as relaxation of the ventricle worsens, this speed falls. You should observe the the E' wave is > A' wave. As relaxation worsens the E' wave will continue to decrease and will fall below 8 cm/s (A' will initially increase and then decrease as disease progresses).
Now that you have performed your ultrasound (and saved your images with waveforms), a useful number to calculate to determine if diastolic dysfunction is contributing to your patient's symptoms is the left ventricular end diastolic pressure/pulmonary capillary wedge pressure, which is the ratio of E/E'. This number should be < 8 in normal diastolic function. Elevated filling pressure > 15. A number in between 8 and 15 is a grey zone and you should use your clinical gestalt here.
Diastolic failure can occur with normal systolic function up to 50% of the time so make sure to keep this on your differential. Patients will present along a spectrum of disease, from normal to a restrictive pattern and ultrasound will help with identifying where patients are along this continuum. Diastolic function is dynamic and even once a patient reaches a restrictive pattern, with aggressive diuresis they can move leftward along the spectrum back to less severe disease. This makes ultrasound useful for monitoring treatment efficacy as well.
Be sure to first get an overall gestalt of cardiac function, including chamber size. Use mitral inflow to evaluate E and A waves. Tissue doppler will then assist with assessing LV relaxation properties, differentiating between normal and pseudo-normal patterns, as well as determining the LVEDP/PCWP. Lastly, be sure to incorporate your ultrasound findings into the overall clinical picture and don't anchor on an ultrasound finding if it just doesn't fit!
THAT'S IT FOR THIS WEEK
If you are interested in learning more about the ULA learning experience, visit their website below:
More on diastology can be found in "Introduction to Bedside Ultrasound," Volume 1 & 2, from Dr. Mallin and Dr. Dawson. If you are interested in purchasing these ebooks for less than $1, visit Ultrasound Podcast Consumables.
- Ultrasound Leadership Academy Diastology Lectures
- Paulus et al. How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. European Heart Journal (2007) 28, 2539–2550.
- Nagueh et al. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography. Journal of the American Society of Echocardiography (2009) Vol 22 , 107-133.
- Nazerian et al. Diagnostic Accuracy of Emergency Doppler Echocardiography for Identification of Acute Left Ventricular Heart Failure in Patients with Acute Dyspnea: Comparison with Boston Criteria and N-terminal Prohormone Brain Natriuretic Peptide. Academic Emergency Medicine Journal (2010) Vol 17, 18-26.
- Lilly, Leonard S. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2007. Print.