Ask the Clinical Instructor

Ask the Clinical Instructor: The Frank-Starling Principle

Questions are answered by: Todd Ginapp, EMT-P, RCIS, FSICP Todd is the Cardiology Manager for Memorial Hermann Southeast in Houston, Texas. He also teaches an online RCIS Review course for Spokane Community College, in Spokane, Washington, and regularly presents with RCIS Review Courses.
Questions are answered by: Todd Ginapp, EMT-P, RCIS, FSICP Todd is the Cardiology Manager for Memorial Hermann Southeast in Houston, Texas. He also teaches an online RCIS Review course for Spokane Community College, in Spokane, Washington, and regularly presents with RCIS Review Courses.
“I am new to the cath lab and have been sitting in on some vendor in-services. I’ve heard ‘Frank Starling’ a few times already, and I think it has something to do with heart failure. Can you explain what that is?” – Received at http://www.facebook.com/RCISReview We’ve used that term a few times in previous articles, and you will likely see it in future articles as well. ‘Frank Starling’ comes from 1914 when Otto Frank and Ernest Starling theorized that the length of the sarcomere [cardiac cell] is the driving force behind effective systole.1 Over the years, this has been abbreviated to be called the Frank-Starling Rule of the Heart. You might also see this as “law,” “mechanism” or “principle” (which I will use in this article). It’s all the same. The Frank-Starling Principle states that the greater the volume of blood entering the heart during diastole, the greater the volume of blood ejected during systole. Simply, the heart will pump OUT whatever it receives…to a point. In the normal patient, this means there is a balance between venous return and systolic delivery. To make sense of this, let’s look at a graphic (Figure 1). Here we see aortic waveforms. We see a premature ventricular contraction (PVC) with a compensatory pause. During that pause, there is a longer diastolic filling time. On the next systolic beat after the pause, the pressure of the waveform is higher. This is the Frank-Starling Principle in action. There was a longer diastolic period, allowing more blood to fill the heart, and once filled, the heart ejected everything returned to it, resulting in the higher pressure. Now, in Figure 2, we can see a negative aspect of the Frank-Starling Principle. The Frank-Starling Principle is still at work here. The heart rate is fast, and the diastolic period is reduced. Therefore, not much blood is filling the ventricles because of that reduced period of time. That’s why we see gradually decreasing pressures, because the heart can’t fill up properly because there isn’t enough time to do so. It’s not until there is a pause in the cycle, allowing just slightly more filling during diastole, that the pressure increases. And, as you can see, the tachycardia continues with the corresponding reduction in aortic (AO) pressures. Remember the equation Cardiac Output = Heart Rate x Stroke Volume (CO = HR x SV). In this case, the reduced filling pressures correlate to a decrease in stroke volume (amount pumped out of the heart with systole). If we decrease stroke volume, we will see a decrease in cardiac output and a decrease in blood pressure. In the beginning of the article, I mentioned that the Frank-Starling Principle works “to a point.” The Frank-Starling Principle is all about the stretching of the sarcomere and the subsequent tension created, allowing a “snap-back” of the heart cell(s) to their normal position. Think of it as a large rubber band. When it is a new rubber band, no matter how far out you stretch it, it will return to its normal position (unless you break it, of course). However, if you continually stretch it out too far, too often (let’s say years), eventually it will stretch out and begin to lose its elasticity and not return to its normal shape. If that is continued, eventually the rubber band will lose all its elasticity, become floppy, and not stretch nor return to its normal shape. The heart can do the exact same thing if it is constantly is trying to pump out all the blood returned to it, such as in congestive heart failure (CHF). At some point, the sarcomeres become weak because they have been maximally stretched out for too long. The heart can no longer pump out everything that is returned to it (hence the “to a point” comment) and constantly stays in a “deficit” and becomes volume overloaded. This cycle continues and heart failure worsens. That is a topic for another article. I hope that you now understand this hemodynamic principle and can apply it to the many pathologies and patient care issues in which this principle is involved. Next month, we’ll talk about a pathology somewhat related to this topic, the Brockenbrough Sign. Contact “Ask the Clinical Instructor” with your question at tginapp@rcisreview.com or on Facebook at www.facebook.com/RCISReview. Reference 1. Starling, EH. The Linacre Lecture on the Law of the Heart (Cambridge, 1915). London: Longmans, Green & Company, 1918.
References
NULL