What happens to stroke volume when blood volume decreases?

Gravitational forces significantly affect venous return, cardiac output, and arterial and venous pressures. To illustrate this, consider a person who is lying down and then suddenly stands up. When the person is lying down (supine position), gravitational forces are similar on the thorax, abdomen and legs because these compartments lie in the same horizontal plane. In this position, venous blood volumes and pressures are distributed evenly throughout the body. When the person suddenly stands upright, gravity acts on the vascular volume causing blood to accumulate in the lower extremities. (Compare the size of veins in the top of your feet while lying down and standing.) Because venous compliance is high and the veins readily expand with blood, most of the blood volume shift occurs in the veins. Therefore, venous volume (Vol) and pressure (VP) become very high in the feet and lower limbs when standing. This shift in blood volume decreases thoracic venous blood volume (CV Vol) and therefore central venous pressure (CVP) decreases. This decreases right ventricular filling pressure (preload), leading to a decline in stroke volume by the Frank-Starling mechanism. Left ventricular stroke volume also falls because of reduced pulmonary venous return (decreased left ventricular preload). This causes cardiac output (CO) and mean arterial pressure (MAP) to fall. If arterial pressure falls appreciably upon standing, this is termed orthostatic or postural hypotension.This fall in arterial pressure can reduce cerebral blood flow to the point where a person might experience syncope (fainting).

Table of Contents Show

Regulation of Blood Volume by Renal Excretion of Water and Sodium
How Blood Volume Affects Blood Pressure
Preload and afterload
Stroke volume index

When a person stands up, baroreceptor reflexes are rapidly activated to restore arterial pressure so that mean arterial pressure normally is not reduced by more than a few mmHg when a person is standing compared to lying down. However, in order to maintain this normal mean arterial pressure, the person who is standing upright has increased systemic vascular resistance (sympathetic mediated), decreased venous compliance (due to sympathetic activation of veins), decreased stroke volume (due to decreased preload), and increased heart rate (baroreceptor-mediated tachycardia). Patients with autonomic nerve dysfunction or hypovolemia will not be able effectively utilize these compensatory mechanisms and therefore will display orthostatic hypotension.

Without the operation of important compensatory mechanisms, standing upright would lead to significant edema in the feet and lower legs in addition to orthostatic hypotension. Venous pooling and reduced venous return are rapidly compensated in a normal individual by neurogenic vasoconstriction of veins, the functioning of venous valves, by muscle pump activity, and by the abdominothoracic pump. When these mechanisms are operating, capillary and venous pressures in the feet will only be elevated by 10-20 mmHg, mean aortic pressure will be maintained, and central venous pressure will be only slightly reduced.

When a standing person suddenly changes to the supine position, gravity no longer causes a shift in blood volume from the thoracic compartment to the legs and feet. Therefore, the blood volume in the thoracic (central venous) compartment as blood volume shift away from the legs. This increases preload on the heart, thereby increasing stroke volume, although the resulting increase in cardiac output will be tempered by a reduction in heart rate through vagal activation and sympathetic withdrawal. Sympathetic activation of the systemic vasculature is also reduced, which causes systemic vascular resistance to fall as the resistance vessels dilate.

Revised 12/7/16

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

Blood volume is determined by the amount of water and sodium ingested, excreted by the kidneys into the urine, and lost through the gastrointestinal tract, lungs and skin. The amounts of water and sodium ingested and lost are highly variable. To maintain blood volume within a normal range, the kidneys regulate the amount of water and sodium lost into the urine. For example, if excessive water and sodium are ingested, the kidneys normally respond by excreting more water and sodium into the urine. The details of how the kidneys handle water and sodium are beyond the scope of this cardiovascular web site; therefore, the reader is encouraged to consult general medical physiology textbooks to learn more about this topic. The following paragraphs briefly describe how renal excretion of water and sodium are regulated and how blood volume affects cardiovascular function.

Regulation of Blood Volume by Renal Excretion of Water and Sodium

Blood is filtered at the glomerulus. This filtrate contains sodium, water and other substances. As the filtrate travels through the proximal tubule, loop of Henle, distal and collecting tubules, the concentration of sodium is altered by transport of sodium across the tubular wall and into the renal interstitium, where it can diffuse into a dense network of intrarenal capillaries. Some of the renal tubules are permeable to water, so water leaves those tubular regions along with the sodium.

The primary mechanism by which the kidneys regulate blood volume is by adjusting the amount of water and sodium lost into the urine. At different sites along the proximal tubules, thick ascending limb of the loop of Henle, distal and collecting tubules, sodium transport is regulated by angiotensin II (Ang II), which increases sodium transport thereby leading to sodium retention. In the collecting tubules, another hormone (aldosterone), stimulates sodium transport from the tubular fluid into the interstitium. Together, Ang II and aldosterone provide a powerful mechanism for increasing sodium retention and consequently fluid volume in the body. A third hormone, antidiuretic hormone (ADH), increases water permeability in the late distal tubules and collecting tubules. This enables water to diffuse from the tubulular fluid into the hypertonic interstitium, thereby reducing urine volume and therefore water loss. Beside these hormone actions on sodium transport and water movement, changes in renal blood flow and glomerular filtration can affect the amount of sodium and water filtered at the glomerulus and entering the renal tubules. For example, increased blood volume increases arterial pressure, renal perfusion, and glomerular filtration rate. This leads to an increase in renal excretion of water and sodium that is termed pressure natriuresis. In certain types of renal disease, the pressure natriuresis relationship is altered so that the kidneys retain more sodium and water at a given pressure, thereby increasing blood volume.

Activation of the renin-angiotensin-aldosterone (RAAS) system causes increased sodium retention by the kidneys, which leads to reduced water loss into the urine and therefore blood volume expansion. RAAS activation occurs during heart failure, which leads to fluid retention in the body. RAAS activation also occurs with renal artery stenosis, which is one cause of secondary hypertension. Drugs that block the formation of angiotensin II (i.e., angiotensin converting enzyme inhibitors), or block aldosterone receptors (e.g., spironolactone) enhance sodium and water loss, and thereby reduce blood volume. Therefore, any mechanism or drug that alters the activity of the renin-angiotensin-aldosterone system will affect blood volume.

How Blood Volume Affects Blood Pressure

Changes in blood volume affect arterial pressure by changing cardiac output. An increase in blood volume increases central venous pressure. This increases right atrial pressure, right ventricular end-diastolic pressure and volume. This increase in ventricular preload increases ventricular stroke volume by the Frank-Starling mechanism. An increase in right ventricular stroke volume increases pulmonary venous blood flow to the left ventricular, thereby increasing left ventricular preload and stroke volume. An increase in stroke volume then increases cardiac output and arterial blood pressure.

Revised 4/25/2014

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from the left ventricle per beat. Stroke volume is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat (called end-systolic volume[note 1]) from the volume of blood just prior to the beat (called end-diastolic volume). The term stroke volume can apply to each of the two ventricles of the heart, although it usually refers to the left ventricle. The stroke volumes for each ventricle are generally equal, both being approximately 70 mL in a healthy 70-kg man.

Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate, and is also used to calculate ejection fraction, which is stroke volume divided by end-diastolic volume. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function.[citation needed]

Example values in healthy 70-kg man

Ventricular volumes view talk edit
Measure	Right ventricle	Left ventricle
End-diastolic volume	144 mL(± 23 mL)[1]	142 mL (± 21 mL)[2]
End-diastolic volume / body surface area (mL/m2)	78 mL/m2 (± 11 mL/m2)[1]	78 mL/m2 (± 8.8 mL/m2)[2]
End-systolic volume	50 mL (± 14 mL)[1]	47 mL (± 10 mL)[2]
End-systolic volume / body surface area (mL/m2)	27 mL/m2 (± 7 mL/m2)[1]	26 mL/m2 (± 5.1 mL/m2)[2]
Stroke volume	94 mL (± 15 mL)[1]	95 mL (± 14 mL)[2]
Stroke volume / body surface area (mL/m2)	51 mL/m2 (± 7 mL/m2)[1]	52 mL/m2 (± 6.2 mL/m2)[2]
Ejection fraction	66% (± 6%)[1]	67% (± 4.6%)[2]
Heart rate	60–100 bpm[3]	60–100 bpm[3]
Cardiac output	4.0–8.0 L/minute[4]	4.0–8.0 l L/minute[4]

Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle.

S V = E D V − E S V {\displaystyle SV=EDV-ESV}

In a healthy 70-kg man, ESV is approximately 50 mL and EDV is approximately 120mL, giving a difference of 70 mL for the stroke volume.

Stroke work refers to the work, or pressure of the blood ("P") multiplied by the stroke volume.[5] ESV and EDV are fixed variables. Heart rate and Stroke volume are unfixed.

Major factors influencing stroke volume – Multiple factors impact preload, afterload, and contractility, and are the major considerations influencing SV.[6]

Men, on average, have higher stroke volumes than women due to the larger size of their hearts.[7] However, stroke volume depends on several factors such as heart size, contractility, duration of contraction, preload (end-diastolic volume), and afterload. Corresponding to the oxygen uptake, women's need for blood flow does not decrease and a higher cardiac frequency makes up for their smaller stroke volume.[7]

Exercise

Prolonged aerobic exercise training may also increase stroke volume, which frequently results in a lower (resting) heart rate. Reduced heart rate prolongs ventricular diastole (filling), increasing end-diastolic volume, and ultimately allowing more blood to be ejected.[8]

Preload and afterload

Stroke volume is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting). An increase in the volume or speed of venous return will increase preload and, through the Frank–Starling law of the heart, will increase stroke volume. Decreased venous return has the opposite effect, causing a reduction in stroke volume.[9]

Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume. It usually does not affect stroke volume in healthy individuals, but increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume. Increased afterload may be found in aortic stenosis and arterial hypertension.[10]

Stroke volume index

Similar to cardiac index, stroke volume index is a method of relating the stroke volume (SV) to the size of the person body surface area (BSA).

$S V I = S V B S A = ( C O / H R ) B S A = C O H R × B S A {\displaystyle SVI={SV \over BSA}={(CO/HR) \over BSA}={CO \over {HR\times BSA}}}$

^ In short, the remaining blood volume left in the left ventricle not pumped out after a systole.

^ a b c d e f g Maceira AM, Prasad SK, Khan M, Pennell DJ (December 2006). "Reference right ventricular systolic and diastolic function normalized to age, gender and body surface area from steady-state free precession cardiovascular magnetic resonance" (PDF). European Heart Journal. 27 (23): 2879–88. doi:10.1093/eurheartj/ehl336. PMID 17088316.
^ a b c d e f g Maceira A (2006). "Normalized Left Ventricular Systolic and Diastolic Function by Steady State Free Precession Cardiovascular Magnetic Resonance". Journal of Cardiovascular Magnetic Resonance. 8: 417–426. doi:10.1080/10976640600572889. (subscription required)
^ a b Normal ranges for heart rate are among the narrowest limits between bradycardia and tachycardia. See the Bradycardia and Tachycardia articles for more detailed limits.
^ a b "Normal Hemodynamic Parameters – Adult" (PDF). Edwards Lifesciences LLC. 2009.
^ Katz AM (2006). Physiology of the heart. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 337. ISBN 0-7817-5501-8.
^ Betts JG (2013). Anatomy & physiology. pp. 787–846. ISBN 978-1938168130. Retrieved 11 August 2014.
^ a b Cotes, John E.; Maynard, Robert L.; Pearce, Sarah J.; Nemery, Benoit B.; Wagner, Peter D.; Cooper, Brendan G. (2020). Lung Function. John Wiley & Sons. p. 450. ISBN 9781118597354.
^ Clancy, John; McVicar, Andrew (2017). Physiology and Anatomy for Nurses and Healthcare Practitioners: A Homeostatic Approach, Third Edition. CRC Press. p. 336. ISBN 1444165283.
^ Chang, David W. (2013). Clinical Application of Mechanical Ventilation. Cengage Learning. p. 31. ISBN 1285667344.
^ Pocock, Gillian; Richards, Christopher D.; Richards, David A. (2018). Human Physiology. Oxford University Press. p. 437. ISBN 019873722X.

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Boron WF, Boulpaep EL (2005). Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA: Elsevier/Saunders. ISBN 1-4160-2328-3.