What is the relationship between blood pressure and cardiac output blood volume and peripheral resistance?

Chapter 5: Blood Pressure

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Cardiac Output
Peripheral Vascular Resistance
Volume of Circulating Blood
Viscosity of Blood
Elasticity of Vessel Walls

Five factors influence blood pressure:

Cardiac output
Peripheral vascular resistance
Volume of circulating blood
Viscosity of blood
Elasticity of vessels walls

Blood pressure increases with increased cardiac output, peripheral vascular resistance, volume of blood, viscosity of blood and rigidity of vessel walls.

Blood pressure decreases with decreased cardiac output, peripheral vascular resistance, volume of blood, viscosity of blood and elasticity of vessel walls.

Cardiac Output

Cardiac output is the volume of blood flow from the heart through the ventricles, and is usually measured in litres per minute (L/min). Cardiac output can be calculated by the stroke volume multiplied by the heart rate. Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow. These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels. Conversely, any factor that decreases cardiac output, by decreasing heart rate or stroke volume or both, will decrease arterial pressure and blood flow. These factors include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis.

Peripheral Vascular Resistance

Peripheral vascular resistance refers to compliance, which is the ability of any compartment to expand to accommodate increased content. A metal pipe, for example, is not compliant, whereas a balloon is. The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure. Veins are more compliant than arteries and can expand to hold more blood. When vascular disease causes stiffening of arteries (e.g., atherosclerosis or arteriosclerosis), compliance is reduced and resistance to blood flow is increased. The result is more turbulence, higher pressure within the vessel, and reduced blood flow. This increases the work of the heart.

Volume of Circulating Blood

Volume of circulating blood is the amount of blood moving through the body. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. Baroreceptors are pressure-sensing receptors. As the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac centre responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is also true.

Viscosity of Blood

Viscosity of blood is a measure of the blood’s thickness and is influenced by the presence of plasma proteins and formed elements in the blood. Blood is viscous and somewhat sticky to the touch. It has a viscosity approximately five times greater than water. Viscosity is a measure of a fluid’s thickness or resistance to flow, and is influenced by the presence of the plasma proteins and formed elements within the blood. The viscosity of blood has a dramatic effect on blood pressure and flow. Consider the difference in flow between water and honey. The more viscous honey would demonstrate a greater resistance to flow than the less viscous water. The same principle applies to blood.

Elasticity of Vessel Walls

Elasticity of vessel walls refers to the capacity to resume its normal shape after stretching and compressing. Vessels larger than 10 mm in diameter are typically elastic. Their abundant elastic fibres allow them to expand as blood pumped from the ventricles passes through them, and then to recoil after the surge has passed. If artery walls were rigid and unable to expand and recoil, their resistance to blood flow would greatly increase and blood pressure would rise to even higher levels, which would in turn require the heart to pump harder to increase the volume of blood expelled by each pump (the stroke volume) and maintain adequate pressure and flow. Artery walls would have to become even thicker in response to this increased pressure.

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Magder SA. The highs and lows of blood pressure: toward meaningful clinical targets in patients with shock. Crit Care Med. 2014;42(5):1241–51.
Article Google Scholar
Dobrin PB. Mechanical properties of arteries. Physiol Rev. 1978;58(2):397–460.
CAS Article Google Scholar
Roach MR, Burton AC. The reason for the shape of the distensibility curves of arteries. Can J Biochem Physiol. 1957;35(8):681–90.
CAS Article Google Scholar
Burton AC. The vascular bed. Physiology and biophysics of the circulation. Chicago: Year Book Medical Publishers Inc.; 1965. p. 61–92.

Google Scholar
Burton AC. On the physical equilibrium of small blood vessels. Am J Physiol. 1951;164:319–29.
CAS PubMed Google Scholar
Azuma T, Oka S. Mechanical equilibrium of blood vessel walls. Am J Physiol. 1971;221:1210–318.
Google Scholar
Oka S, Azuma T. Physical theory of tension in thick-walled blood vessels in equilibrium. Biorheology. 1970;7:109–17.
CAS Article Google Scholar
Burton AC. Total fluid energy, gravitational potential energy, effects of posture. physiology and biophysics of the circulation: an introductory text. Chicago: Year Book Medical Publishers Inc.; 1965. p. 95–111.
Google Scholar
Magder S. Is all on the level? Hemodynamics during supine versus prone ventilation. Am J Respir Crit Care Med. 2013;188(12):1390–1.
Article Google Scholar
Magder SA. Pressure-flow relations of diaphragm and vital organs with nitroprusside-induced vasodilation. J Appl Physiol. 1986;61:409–16.
CAS Article Google Scholar
Permutt S, Riley S. Hemodynamics of collapsible vessels with tone: the vascular waterfall. J Appl Physiol. 1963;18(5):924–32.
CAS Article Google Scholar
Sylvester JL, Traystman RJ, Permutt S. Effects of hypoxia on the closing pressure of the canine systemic arterial circulation. Circ Res. 1981;49:980–7.
CAS Article Google Scholar
Kato R, Pinsky MR. Personalizing blood pressure management in septic shock. Ann Intensive Care. 2015;5(1):41.
Article Google Scholar
Magder S. Starling resistor versus compliance. Which explains the zero-flow pressure of a dynamic arterial pressure-flow relation? Circ Res. 1990;67:209–20.
CAS Article Google Scholar
Bellamy RF. Diastolic coronary artery pressure-flow relations in the dog. Circ Res. 1978;43(1):92–101.
CAS Article Google Scholar
Shrier I, Hussain SNA, Magder S. Effect of carotid sinus stimulation on resistance and critical closing pressure of the canine hindlimb. Am J Physiol. 1993;264:H1560–H6.
CAS PubMed Google Scholar
Shrier I, Magder S. NG-nitro-L-arginine and phenylephrine have similar effects on the vascular waterfall in the canine hindlimb. Am J Physiol. 1995;78(2):478–82.
CAS Google Scholar
Shrier I, Magder S. Response of arterial resistance and critical closing pressure to change in perfusion pressure in canine hindlimb. Am J Physiol. 1993;265:H1939–H45.
CAS PubMed Google Scholar
Shrier I, Magder S. The effects of nifedipine on the vascular waterfall and arterial resistance in the canine hindlimb. Am J Physiol. 1995;268:H372–H6.
Google Scholar
Shrier I, Magder S. Effects of adenosine on the pressure-flow relationships in an in vitro model of compartment syndrome. J Appl Physiol. 1997;82(3):755–9.
CAS Article Google Scholar
Sagawa K. The ventricular pressure-volume diagram revisited. Circ Res. 1978;43:677–87.
CAS Article Google Scholar
Suga H, Saeki Y, Sagawa K. End-systolic force-length relationship of nonexcised canine papillary muscle. Am J Phys. 1977;233(6):H711–H7.
CAS Google Scholar
Guarracino F, Baldassarri R, Pinsky MR. Ventriculo-arterial decoupling in acutely altered hemodynamic states. Crit Care. 2013;17(2):213.
Article Google Scholar
Wang JJ, O'Brien AB, Shrive NG, Parker KH, Tyberg JV. Time-domain representation of ventricular-arterial coupling as a windkessel and wave system. Am J Physiol Heart Circ Physiol. 2003;284(4):H1358–68.
CAS Article Google Scholar
Monge Garcia MI, Gil Cano A, Gracia Romero M. Dynamic arterial elastance to predict arterial pressure response to volume loading in preload-dependent patients. Crit Care. 2011;15(1):R15.

Article Google Scholar
Cecconi M, Monge Garcia MI, Gracia Romero M, Mellinghoff J, Caliandro F, Grounds RM, et al. The use of pulse pressure variation and stroke volume variation in spontaneously breathing patients to assess dynamic arterial elastance and to predict arterial pressure response to fluid administration. Anesth Analg. 2015;120(1):76–84.
Article Google Scholar
Garcia MI, Romero MG, Cano AG, Aya HD, Rhodes A, Grounds RM, et al. Dynamic arterial elastance as a predictor of arterial pressure response to fluid administration: a validation study. Crit Care. 2014;18(6):626.
Article Google Scholar
Pinsky MR. Defining the boundaries of bedside pulse contour analysis: dynamic arterial elastance. Crit Care. 2011;15(1):120.
Article Google Scholar
Sunagawa K, Maughan WL, Burkhoff D, Sagawa K. Left ventricular interaction with arterial load studied in isolated canine ventricle. Am J Phys. 1983;245(5 Pt 1):H773–80.
CAS Google Scholar
Sunagawa K, Maughan WL, Sagawa K. Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle. Circ Res. 1985;56(4):586–95.
CAS Article Google Scholar
Monge Garcia MI, Guijo Gonzalez P, Gracia Romero M, Gil Cano A, Rhodes A, Grounds RM, et al. Effects of arterial load variations on dynamic arterial elastance: an experimental study. Br J Anaesth. 2017;118(6):938–46.
CAS Article Google Scholar
Nakashima T, Tanikawa J. A study of human aortic distensibility with relation to atherosclerosis and aging. Angiology. 1971;22(8):477–90.
CAS Article Google Scholar
Maughan WL, Sunagawa K, Burkhoff D, Graves WL Jr, Hunter WC, Sagawa K. Effect of heart rate on the canine end-systolic pressure-volume relationship. Circulation. 1985;72(3):654–9.
CAS Article Google Scholar
Magder S, Guerard B. Heart-lung interactions and pulmonary buffering: lessons from a computational modeling study. RespirPhysiol Neurobiol. 2012;182(2–3):60–70.
Article Google Scholar
Moncada S, Higgs A. The L-arginine-nitric oxide pathway. N Engl J Med. 1993;329(27):2002–12.
CAS Article Google Scholar
Johnson PC. Autoregulation of blood flow. Circ Res. 1986;59:483–95.
CAS Article Google Scholar
Magder S. Phenylephrine and tangible bias. Anesthesia Analgesia. 2011;113(2):211–3.
Article Google Scholar
Hainsworth R, Karim F, McGregor KH, Rankin AJ. Effects of stimulation of aortic chemoreceptors on abdominal vascular resistance and capacitance in anaesthetized dogs. J Physiol. 1983;334:421–31.
CAS Article Google Scholar
Deschamps A, Magder S. Baroreflex control of regional capacitance and blood flow distribution with or without alpha adrenergic blockade. J Appl Physiol. 1992;263:H1755–H63.
CAS Google Scholar
Magder S. Volume and its relationship to cardiac output and venous return. Crit Care. 2016;20:271.
CAS Article Google Scholar
Krogh A. The regulation of the supply of blood to the right heart. Skand Arch Physiol. 1912;27:227–48.
Article Google Scholar
Thiele RH, Nemergut EC, Lynch C III. The physiologic implications of isolated alpha 1 adrenergic stimulation. Anesth Analg. 2011;113(2):284–96.
CAS Article Google Scholar
Datta P, Magder S. Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia. Am J Resp Crit Care Med. 1999;160(6):1987–93.
CAS Article Google Scholar
Furchgott RF, Zawadzki JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature. 1980;288:373–6.
CAS Article Google Scholar
Moncada S. The L-arginine:nitric oxide pathway. Acta Physiol Scand. 1992;145:201–27.
CAS Article Google Scholar

Page 2

Effect of age and initial volume on thoracic aortic elastance. The slopes of the lines are elastance. The right upper insert shows the increase in circumferential tension versus increases in aortic circumference in percent for age < 18 to > 80 years [33]. The lower left shows a schematic pressure–volume relationship for the aorta. The boxes represent stroke volumes. The same stroke volume A starting from the same initial volume produces increasing pulse pressures depending upon the shape and position of the start of the stroke volume. The stroke volume B is the same size as in A but starts at a higher initial volume and produces a much larger pulse pressure