So I have looked all over this site for information regarding afterload...and everywhere else!!! I have been trying to get this question answered for a while now and I can't seem to get it to where I'm satisfied with the answer.
There is a burn pt. his propane tank exploded burning the face, arms, and chest. He has mixed burns to most areas except his hands and face where he has 3rd degree burns. His BP is 65/45 and his HR is 200 bpm. He was unconscious in the ER but regained consciousness the next day.
Now I have to explain why his BP is so low using the BP equation and why his HR is so high using the BP equation.
Now my book says the BP equation is: BP = CO x PR. TPR is the total resistance for the systemic circulation, so TPR is often referred to as SVR. Now the equation for CO is: CO = SV x HR. SV is determined by preload, afterload, and contractility. HR is mainly regulated by the PNS and the SNS. Now the patient has burns so he is going to have fluid shifts (third-spacing), which leads to hypovolemic shock. As a result the BV decreases. The decreased BV causes decreased venous return to the heart, which means preload decreases. With less blood coming back to the heart, the heart contracts less because it has less blood to push out. Therefore, less blood to eject means that SV decreases. Since CO is a product of SV and HR, as a result of a decreased SV, CO will decrease. Also, CO is the amount of blood ejected from the heart per minute (per cycle). Therefore, if the heart beats less times per minute, less blood is leaving, which results in a decreased CO. Since BP is the product of CO and PR, a decrease in CO will result in a corresponding decrease in BP. However, the body quickly responds to the decreased BV and BP by activating the SNS, which leads to an increase in HR and contractility, and causes peripheral vasoconstriction (so blood is shunted from the less-vital areas - like the skin and GI tract - to the more vital areas - like the heart and brain). This should cause BP to increase back to normal. Because again, CO is the product of HR and SV. An increase in HR causes CO to increase. The peripheral vasoconstriction causes afterload to increase, which causes SV to increase. BP is the product of CO and PR. Therefore, BP increases to normal.
However, the patient's BP is so low that this tells me that the compensatory mechanisms are no longer working. I get kind of lost here. Because his HR is high, so it makes me think that his compensatory mechanisms are still working. Also, he was unconscious in the ER, but regained consciousness the next day. That tells me that the perfusion to his brain decreased enough to make him unconscious, but the perfusion increased enough for him to regain consciousness. I'm not sure if that's right - if that's why he lost consciousness and regained consciousness again? OK back to the HR. I know that when the HR is excessive enough - like 200 bpm - it decreases the amount of filling time (time in diastole). the heart does not remain relaxed (in diastole) long enough to allow the cardiac chambers enough time to be completely filled before the next contraction. This causes EDV to be decreased, which results in a decrease in preload. The decreased preload leads to a decrease in SV. As a result, CO no longer increases but falls. Also, with such an excessive HR resulting in less diastolic filling time and decreased EDV, there is less ventricular wall stretch. According to Frank-Starling mechanism, less wall stretch means that you have less contractility. So you have increased HR, but you have myocardial depression (poor contractility). I think that's right. OK so you have an excessive HR - I think due to the SNS trying to raise the BP, but eventually the compensatory mechanisms become detrimental to the person. The increased HR, vasoconstriction (increased afterload) cause more harm than good. So the HR becomes too high and results in the CO decreasing. The decreased CO causes the BP to decrease.
So the HR is so high and the BP is low because the HR increases as a compensatory mechanism to maintain BP, however it eventually starts to do more harm than good. The HR increases to an excessive amount, where the heart does not have enough time to fill properly. This causes the CO to decrease, which leads to a corresponding decrease in BP.
OK sorry...I seem to have gotten off the point of my question. I actually have 2 questions I guess. To see if I am right regarding this case and regarding afterload. Now on to afterload.
So my teacher in his lecture said that afterload is the force that the heart has to push against. So he gave 2 examples. I think I get it but want to make sure
For example, if you have a mean pressure in the aorta of 100 mmHg, you must generate what is known as the afterload - you must generate a force in excess of 100 mmHg in order to open up the aortic valve.
So I understood this as - He said that afterload is the force the heart has to push against. So if the mean pressure in the aorta is 100 mmHg. The blood is in the left ventricle. So in order for the aortic valve to open up and for the blood to be pushed through and into the aorta and out to the rest of the body a force in excess of 100 mmHg must be generated. He said that you must generate what is known as the afterload - you must generate a force in excess of 100 mmHg to open up the aortic valve and get the blood through to be dispersed to the body. So for example, so a force of 150 mmHg is generated in order to open up the aortic valve. Then what he is saying is that the 150 mmHg, for example, would be the afterload.
Second Example:
If we're talking about the pulmonary circuit, in the pulmonary trunk, the mean BP is about 20 mmHg, so that would be the afterload in the pulmonary system. So you have to generate a force in excess of 20 mmHg to open up the pulmonary valve.
So I understand this as - Again, he said afterload is the force the heart has to push against. So if the mean pressure in the pulmonary artery is 20 mmHg he is saying that is the afterload. He said "the mean BP is about 20 mmHg, so that would be the afterload in the pulmonary system." So the heart would have to push against the 20 mmHg in order to get the pulmonary valve open and get the blood through to go to the lungs. This is what I think is afterload. If it is the force the heart has to push against. If the pressure in the pulmonary artery is 20 mmHg, unless a force in excess of 20 mmHg is generated that will fight that 20 mmHg and get that valve open, the 20 mmHg of the pulmonary artery will be able to keep that valve closed. So if, for example, the heart generates a force of 40 mmHg, that would be enough force to overcome the force of the pulmonary artery (20 mmHg) and get the pulmonary valve to open and get the blood through to the lungs.
Am I getting this right?
Thanks so much for any help!!!
