The control of the heart rate and stroke volume acts to decrease or increase blood flow in the human body. The volume of blood in people’s heart pumps every minute called cardiac output (CO) fluctuates with the demand they put on their bodies. CO can be computed mathematically using a developed formula, which is just the multiplication of stroke volume (SV) and heart rate (HR). Importantly, the cardiac output of individual’s heart is frequently changing amount that modifies to any emotional or physical demand put on the body. Proper understanding of this situation calls for the need of explaining the control of heart rate and stroke volume in response to changes in the blood gases and blood pressure. First, when explaining the control of heart rate in response to changes in the blood gases and blood pressure, people should know the automatic pacesetter can make the heart to beat on its own in the absence of any external influence. In most cases, the autonomic nervous system tends to change the heart rate for short episodes. According to Iaizzo and Fitzgerald (2015), the autonomic nervous system is normally the separation of nervous system, which is under involuntary control. Also, it is divided into two; the parasympathetic division and sympathetic division (fight-or-flight division). Therefore, when exercising, the nerves of the sympathetic division initiate the automatic pacesetter to fire more regularly, increasing the heart rate. When people disengage from this activity, the stress decreases, making the parasympathetic division of the autonomic nervous system to force the heart to readapt back to a normal resting heart rate. Sympathetic nervous system and parasympathetic nervous system increases and decreases heart rate, respectively. Secondly, the control of stroke volume in response to changes in the blood gases and blood pressure takes place in a diverse manner from that of the heart rate. Skytioti, Søvik, and Elstad (2018) emphasized that stroke volume is the amount of blood pumped during each heartbeat. During the control of stroke volume, end-diastolic volume is realised when the volume of blood in the ventricles occurs at the end of diastole. In this regard, an increase in end-diastolic volume contributes towards more stretching of the ventricles due to the presence of more blood. During this time, Central venous pressure (CVP) may emerge since it is likely to reflect the amount of blood returning to the heart and the capability of the latter to pump it back into arteries. Magder (2015) supported this claim by highlighting that the changes to CVP leads towards fluctuation of the diastolic filling pressure. Added that Magder (2016) Starling’s law of the heart can be relied upon to indicate that when the diastolic filling pressure is increased, there is a rise in the amount of blood available to be pumped out; hence, causing an effective control of stroke volume. In conclusion, the human body encounters various biological processes that support life. This claim can be depicted through the desсrіption how the heart rate and stroke volume is controlled in response to changes in the blood gases and blood pressure. Specifically, the autonomic nervous system plays a vital role in regulating heart rate through the assistance of the automatic pacesetter. On the other hand, stroke volume is controlled when there is an increase and decrease in end-diastolic volume. References Iaizzo, P.A. and Fitzgerald, K.,( 2015). Autonomic nervous system. In Handbook of Cardiac Anatomy, Physiology, and Devices (pp. 235-250). Springer, Cham. Magder, S.,( 2015). Understanding central venous pressure: not a preload index?. Current Opinion in Critical Care, 21(5), pp.369-375. Magder, S. (2016). Volume and its relationship to cardiac output and venous return. Critical Care, [online] 20(1), pp. 1- 11 Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5018186/ [Accessed 11 Dec. 2021]. Skytioti, M., Søvik, S. and Elstad, M. (2018). Respiratory pump maintains cardiac stroke volume during hypovolemia in young, healthy volunteers. Journal of Applied Physiology (Bethesda, Md.: 1985), [online] 124(5), pp.1319–1325. Available at: https://www.ncbi.nlm.nih.gov/pubmed/29494288 [ Accessed 11 Dec 2021].
