Respiratory and Cardio Assignment

 

Heart Control 

Introduction

The ventricles and atria of the heart in human system work together and alternatively by contraction and relaxation to pump the blood through the heart. The electrical system is the power supply in heart controlling the contraction and relaxation system. Heartbeat of the human system is triggered by the electrical impulses. The electrical impulse travels through specialized pathway. Thus the orderly sequence maintained by the heart during heartbeat is as following:

  1. Atrial systole or contraction
  2. Ventricular systole or contraction

Electrical activity of the heart during a heartbeat

The pathway of electrical impulse generating heartbeat is discussed below.

  1. SA node or Sinoatrial node: SA node or sinoatrial node is known as the natural pace maker of human system. The SA node is situated near the junction of the superior vena cava at the right atrium. The electrical impulse initiates in a small bundle with specialized cells in the right atrium (Rossi et al., 2016). This specialized bundle of cells is known as SA node. The electrical activity starts to spread through the wall of the both atrium causing the contraction to them. The contraction results in the blood flow to the ventricles. At that time the SA node determines the rhythm and rate of the heartbeat. Normal rhythm of the heart is called normal sinus rhythm as the SA node generates the fires regularly.
  2. AV node or atrioventricular node: The atrioventricular node or AV node comprises of a cluster of cells and it is situated at the centre of the human heart between the ventricles and the atria. The exact location of the AV node is at the posterior right portion of the inter-atrial septum (Tomasova et al., 2016). The AV node behaves like a gate to slow down the electrical pulse before the pulse enters into the ventricles. The delay in getting the electrical pulse facilitates the atria to get contracted before the contraction of the ventricles.
  3. His-Purkinje Network: The network of His-Purkinje is composed of fibers. Three bundles of fibers from the atrium make the Purkinje-type fibers which connect the SA node and AV node. There is another bundle known as Bachmann bundle used to identify the branch of intermodal tract at the anterior side connecting the left and right atria (Steinvil et al., 2016). The pathway of the fibers sends the electrical impulse to the ventricles. The muscular walls of ventricles take the electrical impulse. Then the contraction of the ventricles takes place. The contraction results in the blood flow out of the heart and entering to the lungs. From the lungs the blood flows to the entire human body (Randles et al., 2015). Atrial myocytes sometimes do the conduction but it is more common in the Purkinje network.
  4. Then the SA node generates another electrical impulse to begin the cardiac cycle again.

The normal heartbeat of the human body at rest is 50 to 99 times per minute. During body activities or exercises or emotions or fever or during medications the heartbeat becomes faster and the heartbeat may become 100 in a minute.

 

Figure 1: Circulatory system

(Source Hyland et al., 2018)

Explanation of pulse rate control by autonomic nervous system

The heart rate of the human body is expressed by the SA node, the natural pace maker of the cardiac muscles. The pacing rate of SA node in the absence of any influences is 100 bpm (beats per minute). The cardiac output and heart rate is able to vary depending on the responses of the body. The SA node influencers, nerve impulses, and hormones have the effects on the speed of the electrical impulses generated by the SA node (Hyland et al., 2018).  This effectively acts on the heart rate (chronotrophy) alterations affecting the cardiac output. The cardiovascular system controls the circulation of blood throughout the human body to supply oxygen and nutrients to the body parts removing the waste products. There are two branches of autonomic (involuntary) nervous system that control the heart rate (Duke et al., 2016). The two branches are sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). The SNS releases the hormones such as catecholamine, epinephrine, and nor epinephrine to enhance the heart rate. The PNS releases hormone acetylcholine to lower the heart rate (Wiard et al., 2017). There are some factors like caffeine, stress, or excitement that can temporarily faster the heart rate. Meditations or deep breaths can slow down the heart rate gradually.

Parasympathetic nervous system (PNS): The PNS input to the heart occurs via vagus nerve (CN X). Synapses are formed by the vagus nerve with the post-ganglionic cells in both SA node and AV node. At the time of its stimulation the hormone acetylcholine binds to the M2 receptor (Ghersi-Egea et al., 2015). M2 receptor acts to minimize the potential of the pacemaker leading to decreasing heart rate (Marseille et al., 2017). This is called negative effect of chronotrophy.

Sympathetic nervous system (SNS): The SNS input to the heart occurs via the fibers of post-ganglion from sympathetic trunk innervating the SA node and AV node. The fibers release nor-adrenaline hormone. The nor-adrenaline acts on the B1 adreno-receptors to increase the potential of pace maker leading to the increasing heart rate (Fuchs et al., 2016). This is called positive effect of chronotrophy. This would further lead to the increase in the force of contraction.

The parasympathetic input dominates when the person is at rest. It gives normal heart rate about 60 bpm. Any increases in the heart rate are caused by the reduction in PNS outflow and increasing the heart rate via SNS outflow over 100 bpm. If the arterial pressure is detected to be increased, the parasympathetic pathway gets activated to minimize the heart rate. This happens along with the increase in vasodilation of the vessels to minimize or lower the arterial pressure. On the other hand if arterial pressure is detected to be decreased, the sympathetic pathway gets activated to enhance the heart rate (Frederick et al., 2019). This happens along with the increase in vasoconstriction of the vessels to enhance or maximize the arterial pressure.  

The heart rate is also controlled by the hormones. One such hormone is adrenaline which is thereby released from the medulla of the adrenaline glands. Adrenaline can be released to the blood stream at the time when an individual is suffering from stresses (Pessa et al., 2017). The result may be the increasing heart rate.

 

Figure 2: Flow chart of ANS

(Source: Abdi et al., 2015)

Calculations for keeps on pumping

  • Body surface area calculation

Weight-= 210 pounds

Height= 190.5 cm

Multiplying height by weight and dividing by 3600= 5 cm/kg

Square root of 5 = 2.24 m2

  • Cardiac output= (2.24 x 3.2)= 7.168 liter/min
  • Stroke volume= 86.66 lit per beat
  • Stroke volume= 86660 ml per minute

Importance of cardiac output

The normal bodily functions depend upon the blood pumping of the heart at the sufficient rate to maintain continuous and adequate supply of the oxygen as well as other nutrients to the vital organs including brain. Cardiac output determines the amount of blood that the heart pumps in each minute. Cardiac output is important because it is related to the amount of blood supplied to the different organs and parts of the human body (Abdi et al., 2015). It is an important indicator to measure the efficiency of the heart meeting the normal bodily demands for perfusion. According to the physicians the cardiac output can be measured by the following formula:

Cardiac output = stroke volume + heart rate

Stroke volume determines the amount of blood the human heart pumps each time of its beating and the heart rate is the measure of number of heart beats per minute (Kamen et al., 2015). By actual means the stroke volume is the quantity of blood released by the left ventricle in one contraction.

Normal cardiac output: Normal cardiac output of a healthy person is 5 - 6 liters of blood per minute when the individual is at rest. The normal cardiac outputs vary among different individuals depending on the sizes.

Requirement of higher cardiac output: Higher cardiac output may be required at the time of exercises or any other bodily activities. The human heart needs four to five time higher cardiac outputs than the normal ones at the time of activities or exercises (Regmi et al., 2017). During the exercises the muscle cells need more oxygen because more amount of blood gets out of the body. The human heart can also increase its stroke volume by pumping the blood forcefully or it can increase the amount of blood filled in the left ventricle before its pumping. Thus the heart beats in both faster as well as stronger way to increase the amount of cardiac output during exercises.

Low cardiac output: Low cardiac output occurs if the human heart cannot pump sufficient blood to the body and tissues. It may result in the heat failure. Large amount of blood loss may also cause low cardiac output (Szyjkowska et al., 2019). The low cardiac output may be caused by severe infection or sepsis and severe damage to the heart.

Thus the maintenance of cardiac output is important because sufficient outputs help in keeping the blood pressure at normal level and it needs to supply blood rich in oxygen to the brain and other important organs.

Cardiac output is dependent on the four factors such as heart rate followed by contractility, preload and lastly the after load. The determination of values of cardiac outputs is dependent on these four components. The clinicians may often consider that the term cardiac output is misleading them by focusing only on the heart, whereas the cardiac output is dependent on both cardiac as well as extra cardiac factors (Gaynullina et al., 2019).  The clinicians tried to understand the individual as well as combined roles of these four factors.

Bar graph showing the blood flow in different organs

 

Figure 3: Blood flow in different organs

(Source-Created by the learner)

Redistribution of blood during exercises and increased blood flow in three organs

The cardio vascular system of the human body redistributes blood during exercises thus more amount of blood goes to the muscles working at the time of exercises. At the same time less amount of blood goes to other body parts (e. g: digestive system). The mechanism of redistribution or redirection of blood is called the vascular shunt mechanism. Short term effect of exercises increase stroke volume, heart rate, cardiac output, and blood pressure.

Organ blood flow can be determined by the expression ml/min. This is the most descriptive unit to express an organ getting supply from an artery or vein. In the animal system the easiest way to measure the organ blood flow is by means of venous outflow in the calibrated container. The organ blood flow can be expressed as the fraction of cardiac output. This fraction can be changed under different pathological conditions such as arterial hypotension, hypoxia, and low cardiac output. The increased blood flow has been observed in heart (atriole and ventricle), lungs, and brain. The maximum amount of blood can be observed in these three organs in due course of circulation (Misra et al., 2017).

Conclusion

The muscle cells get maximum oxygen supply from heart during exercises or heavy work. The heart starts to pump maximum blood. It increases the heart rate. The stroke volume also increases. The pathway becomes normal again when the body come to rest.

 

 

 

References

Abdi, M., Karimi, A., Navidbakhsh, M., Pirzad Jahromi, G. and Hassani, K., 2015. A lumped parameter mathematical model to analyze the effects of tachycardia and bradycardia on the cardiovascular system. International Journal of Numerical Modelling: Electronic Networks, Devices and Fields28(3), pp.346-357.

Duke, J.M., Randall, S.M., Fear, M.W., Boyd, J.H., Rea, S. and Wood, F.M., 2016. Understanding the long-term impacts of burn on the cardiovascular system. Burns42(2), pp.366-374.

Frederick, B., Hocke, L.M. and Tong, Y., Mclean Hospital, 2019. System and method for evaluation of circulatory function. U.S. Patent Application 10/201,314.

Fuchs, D., Wilby, P.R., von Boletzky, S., Abi-Saad, P., Keupp, H. and Iba, Y., 2016. A nearly complete respiratory, circulatory, and excretory system preserved in small Late Cretaceous octopods (Cephalopoda) from Lebanon. PalZ90(2), pp.299-305.

Gaynullina, D.K., Schubert, R. and Tarasova, O.S., 2019. Changes in Endothelial Nitric Oxide Production in Systemic Vessels during Early Ontogenesis—A Key Mechanism for the Perinatal Adaptation of the Circulatory System. International journal of molecular sciences20(6), p.1421.

Ghersi-Egea, J.F., Babikian, A., Blondel, S. and Strazielle, N., 2015. Changes in the cerebrospinal fluid circulatory system of the developing rat: quantitative volumetric analysis and effect on blood-CSF permeability interpretation. Fluids and Barriers of the CNS12(1), p.8.

Hyland, S.L., Hüser, M., Lyu, X., Faltys, M., Merz, T. and Rätsch, G., 2018. Predicting circulatory system deterioration in intensive care unit patients. In AIH@ IJCAI (pp. 87-92).

Kamen, D., Demers, J.A., Altobelli, D.E., Gray, L.B., Perry, N.C., Tracey, B., Dale, J.D., Van der Merwe, D.A. and Owens, K., Deka Products LP, 2015. Heat exchange systems, devices and methods. U.S. Patent 8,968,232.

Marseille, O. and Kerkhoffs, W., CircuLite Inc, 2018. Devices, methods and systems for establishing supplemental blood flow in the circulatory system. U.S. Patent 9,901,667.

Misra, J.C., Sinha, A. and Mallick, B., 2017. Stagnation point flow and heat transfer on a thin porous sheet: Applications to flow dynamics of the circulatory system. Physica A: Statistical Mechanics and its Applications470, pp.330-344.

Pessa, J.E., Kenkel, J.M. and Heldermon, C.D., 2017. Periorbital and temporal anatomy,“targeted fat grafting,” and how a novel circulatory system in human peripheral nerves and brain may help avoid nerve injury and blindness during routine facial augmentation.

Randles, A., Draeger, E.W., Oppelstrup, T., Krauss, L. and Gunnels, J.A., 2015, November. Massively parallel models of the human circulatory system. In Proceedings of the International Conference for High Performance Computing, Networking, Storage and Analysis (p. 1). ACM.

Regmi, S., Fu, A. and Luo, K.Q., 2017. High shear stresses under exercise condition destroy circulating tumor cells in a microfluidic system. Scientific reports7, p.39975.

Rossi, E., Smadja, D.M., Boscolo, E., Langa, C., Arevalo, M.A., Pericacho, M., Gamella-Pozuelo, L., Kauskot, A., Botella, L.M., Gaussem, P. and Bischoff, J., 2016. Endoglin regulates mural cell adhesion in the circulatory system. Cellular and Molecular Life Sciences73(8), pp.1715-1739.

Steinvil, A., Rogers, T., Torguson, R. and Waksman, R., 2016. Overview of the 2016 US Food and Drug Administration circulatory system devices advisory panel meeting on the absorb bioresorbable vascular scaffold system. JACC: Cardiovascular Interventions9(17), pp.1757-1764.

Szyjkowska, A., Gadzicka, E., Szymczak, W. and Bortkiewicz, A., 2019. The reaction of the circulatory system to stress and electromagnetic fields emitted by mobile phones-24-h monitoring of ECG and blood pressure.

Tomasova, L., Konopelski, P. and Ufnal, M., 2016. Gut bacteria and hydrogen sulfide: the new old players in circulatory system homeostasis. Molecules21(11), p.1558.

Wiard, R.M., Giovangrandi, L.B. and Kovacs, G.T., Leland Stanford Junior University, 2017. Systems and methods for monitoring the circulatory system. U.S. Patent 9,833,151.

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