Today, we talk about an important concept in cardiology - consider these tasks while transporting to your local healthcare system:
Giving fluids to right ventricular infarctions
Placing larger doses of NTG under the tongue for patients presenting in CHF
All of the pharmacological interventions above require a deep understanding of cardiac output. To grasp the WHY behind the concepts, one must also take into account the difference between preload and afterload.
As you may recall cardiac output is simply the volume of blood ejected out of the heart every minute. It is a product of both stroke volume and heart rate. [CO= SV X HR], and on average 5L/min leaves our left ventricle every 60 seconds. Cardiac output can be altered or influenced by changes in either variable. If the HR and SV increase, the cardiac output will as well. Output will tend to go down if HR and/or SV decreases. The terms are directly proportional. The heart, as you know is a specialized muscle in that it can generate its own electrical impulse which stimulates contraction (systole) and relaxation (diastole). The atria contract together and then the ventricles contract together. During systole blood leaves each chamber. During diastole blood fills each chamber - this includes the coronary arteries.
During diastole, right before another contraction starts our left ventricle contains some defined volume - meaning the ventricles have an end diastolic volume of around 125-130 ml. A fraction of this volume will leave with every beat. This is your LVLEF or ejection fraction and its simply the quotient of your stroke volume/end diastolic volume [SV/EDV x 100]
All of this math sets the scene for the preload + afterload discussion.
Venous return from the vena cava enters the heart and fills the LV with a defined volume. This volume stretches the walls of the ventricle. At the end of the filling cycle, the degree of stretch on the walls of the ventricle is called PRELOAD. Preload is directly tied to the Frank-Starling mechanism, which states the more you stretch the heart the greater the reflexive contraction of the heart will be.
The degree of resistance encountered by the heart when blood leaves the left ventricle is called AFTERLOAD. It all comes down to fluid dynamics, and the amount of effort it takes to open the semilunar valves. Some resistance will also be present as blood moves through smaller vessels. If you're dual trained as a firefighter/engineer - think about how friction loss works as hose diameters change. The wider the hose or blood vessel - the less resistance. The smaller the hose or blood vessel, the greater the resistance will be. There are lots of things that can contribute to changes in afterload. Some are related to aortic stenosis, while others are centered around atherosclerotic plaque. Around our earlier conversation of stroke volume -- there is an inversely proportional relationship here -- as afterload increases, stroke volume will subsequently decrease.
Some helpful applications are included below - many of which you may already be familiar with:
Increase preload - fluid boluses, exercise, blood transfusions, any type of sympathetic nervous system stimulation. Could be helpful to do this is cases of hypovolemic shock.
Decrease preload - administration of diuretics or nitroglycerin or disease states like Afib with RVR where filling time is significantly impaired.
Increase afterload - disease processes like pulmonary HTN or really anything that promotes vasoconstriction. Now you can understand why untreated HTN causes LVH amongst other things. The LV can only forcefully pump for so long before left heart failure becomes evident.
Decrease afterload - as you can imagine, anything that promotes vasodilation. NTG has implications here as well -- everything is this category will increase/enhance SV.
At the end of the day just remember preload=stretch and afterload=squeeze
November 18, 2024
Author: Joshua Ishmael, MBA, MLS(ASCP)CM, NRP
Pass with PASS, LLC
Comments