Appendix 1: Physical Quantities for Selected Arteries
6.5 Cardiac Remodelling .1 The Remodelling Process
6.4.3 Regulation of the Heart
The Frank–Starling mechanism is an important component of the control of the heart, because any change in end diastolic volume (point A on Fig.6.14) results in a change in cardiac output. This effect is seen very clearly in the way that left ventricular output is balance with right ventricular output. It is crucial that the output from each ventricle is balanced. If there is any sustained difference, then congestion of either pulmonary or systemic circulation follows very quickly.
If there is a transient increase in the output of the right ventricle so that it exceeds the output of the left ventricle, then the volume of blood in the pulmonary circu- lation increases. This increase results in a rise in pulmonary venous pressure, which in turn acts to increase the preload of the left ventricle. The increase in left ven- tricular preload then results, through the Frank–Starling mechanism, in a stronger contraction of the left ventricle, and hence an increase in the left ventricular output.
6.5 Cardiac Remodelling
might include morphological changes, including size of the ventricle and thickness of the wall, and structural changes including re-orientation of thefibres. Increase in the size of the ventricles associated with the pathological response to changed physiological conditions is commonly referred to as ventricular hypertrophy.
There is a large body of clinical literature on ventricular remodelling.
A comprehensive introduction by Cohn et al. (2000) includesfive key consensus statements on concepts of remodelling, remodelling and heart failure progression, diagnostic tools and their clinical value, the effect of therapeutic intervention and educational implications. The focus is on heart failure, and the appreciation of the potential benefits of candidate therapies, particularly pharmacological intervention, based on physiological diagnostic factors including ventricular volume and ejection fraction data. Although the emphasis is on the pathological remodelling associated with disease progression, already in 2000 there is discussion of reverse remodelling as a target for heart failure therapies. A recent state-of-the-art review by Konstam et al. (2011) focuses on measures of remodelling. Several clinical papers discuss the effect on remodelling of candidate surgical interventions to reduce haemodynamic load, e.g. the review by Villa et al. (2006).
6.5.2 Engineering Mechanics of Ventricular Remodelling
The engineering representation of ventricular remodelling is complex because the process is multifactorial. Although the response is essentially an attempt by the heart to maintain performance in terms of cardiac output, and intimately associated with the maintenance of stresses and strain levels in the ventricular wall, there are many genetic factors and biological responses that are outside the normal scope of engineering mechanics. Generally, we recognise the conditions of pressure overload and volume overload as causative factors in the remodelling of the ventricles.
Pressure overload is associated with an excessive afterload on the heart, which means that it has to generate a higher pressure per unitflow. Volume overload is Table 6.2 Typical haemodynamic parameters for a resting 70 kg adult (Levick2009)
Parameter Value at rest
Heart rate 65–75 beats min−1
Stroke volume 70–80 ml
Cardiac output 4.5–6.0 L min−1
Ejection fraction 0.67
Systemic venous pressure 12–15 mmHg
Pulmonary arterial pressure 20–25 mmHg (systole) 8–12 mmHg (diastole)
Pulmonary venous pressure 5–8 mmHg
Systemic aortic pressure 120 mmHg (systole)
80 mHg (diastole)
associated with the size of the heart chamber, referring to the fact that there is an excessive volume of blood at the start of contraction. Of course the two are related, and volume overload might result from long-term pressure overload. The Frank– Starling mechanism, which describes a normal physiological process, has already been discussed earlier in this chapter.
An important review of engineering models of cardiac growth and remodelling (G&R), with emphasis on the remodelling of fibre orientation but including an excellent introduction to the overall concepts, is presented by Bovendeerd (Bovendeerd2012). Bovendeerd’s abstract sums up the challenges:‘A continued effort combining information on mechanotransduction at the cellular level, experi- mental observations on G&R at organ level, and testing of hypotheses on stimulus-effect relations in mathematical models is needed…. Ultimately, models of cardiac G&R seem indispensable for patient-specific modeling, both to reconstruct the actual state of the heart and to assess the long-term effect of potential interventions’. He reviews optimisation models, which compute the cardiac parameters associated with an evolved state of stress and/or strain in end-stage heart failure to characterise the physiological state, and adaptation models which seek to describe the mechanistic relationship between stimulus and effect, describing the evolution in time of tissue and volume properties. Arts et al. (2010) have made major contributions to the develop- ment of models of G&R, from the development four decades ago of singlefibre models of the ventricle, assuming a homogeneous distribution of stress and strain, through to sophisticated patient-specific models including adaptation mechanisms.
References
Arts T, Lumens J, Kroon W, Donker D, Prinzen F, Delhaas T. Patient-specific models of cardiovascular mechanics with a major role for adaptation. In: Kerckhoffs RCP, editor. Patient specific modeling of the cardiovascular system. New York: Springer; 2010. p. 21–41.
Bovendeerd PHM. Modeling of cardiac growth and remodelling of myofiber orientation.
J Biomech. 2012;45:872–81.
Cohn JN, Ferrari R, Sharpe N. Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. Behalf of an international forum on cardiac remodeling. J Am Coll Cardiol. 2000;35:569–82.
Katz AM. Ernest Henry Starling, his predecessors, and the “Law of the Heart”. Circulation.
2002;106:2986–92.
Konstam MA, Kramer DG, Patel AR, Maron MS, Udelson JE. Left ventricular remodeling in heart failure. JACC Cardiovasc Imag. 2011;4:98–108.
Levick RJ. An introduction to cardiovascular physiology. 5th ed. Boca Raton: CRC Press; 2009.
Nielsen P, Le Grice I, Smaill B, Hunter P. Mathematical model of geometry andfibrous structure of the heart. Am J Physiol; Heart Circ Physiol. 1991;260:H1365–78.
Noble D, Rudy Y. Models of cardiac ventricular action potentials: iterative interaction between experiment and simulation. Philos Trans R Soc London; Ser A Math Phys Eng Sci.
2001;359:1127.
Villa E, Troise G, Cirillo M, Brunelli F, Dall Tomba M, Mhagna Z, Tasca G, Quaini E. Cohn JN, Ferrari R, Sharpe N. Factors affecting left ventricular remodelling after valve replacement for aortic stenosis. An overview. Cardiovasc Ultrasound. 2006;4(25). doi:10.1186/1476-7120-4-25.
The Venous System
Andrew J. Narracott
Learning outcomes
1. Describe the role of the venous circulation in providing storage capacity within the circulation.
2. Describe the variation in compliance of the veins with transmural pressure and the implications of this on the resistance toflow as the veins collapse.
3. Describe the features of venous compliance which allow the veins to act as a blood reservoir.
4. Describe the role of the muscle pumps of the lower limb and the respiratory pump in returning blood from the legs to the heart and the importance of venous valves in this process.
5. Describe how the distribution of venous valves varies throughout the circulation.
6. Describe how changes in posture lead to changes in venous volume with attention to the associated timescales.
7. Define what is meant by venous insufficiency and state complications associ- ated with the condition.
8. Describe the applications of B-mode and Doppler ultrasound in diagnosis of venous disease.
9. Describe the features that characterise varicose veins.
10. Describe the nature of deep vein thrombosis (DVT) and the factors associated with increased risk of DVT.
The role of the venous system is to return blood to the heart under low pressure conditions, compared with the arterial system. In humans the haemodynamics of venous flow is significantly influenced by postural changes, due to venous com- pliance, and an understanding of the physics associated with changes in hydrostatic pressure in the veins informs discussion of the biomechanics of the venous system.
A.J. Narracott (&)
Sheffield University, Sheffield, UK e-mail: a.j.narracott@sheffield.ac.uk
©Springer International Publishing Switzerland 2017 P.R. Hoskins et al. (eds.),Cardiovascular Biomechanics, DOI 10.1007/978-3-319-46407-7_7
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This chapter presents key concepts associated with the role of the venous system in the circulation, how these relate to normal physiological conditions and how these processes may be altered under abnormal conditions.