Stroke Volume (SV) is the volume of
blood in millilitres ejected from the each ventricle due to the
contraction of the heart muscle which compresses these ventricles.
SV is the difference between end-diastolic
volume (EDV) and end-systolic volume (ESV). Multiple factors can affect SV, eg.
factors that change either EDV or ESV will change SV. The three primary factors
that regulate SV are preload, afterload and contractility.
Heart rate (HR) also affects SV. Changes
in HR alone inversely affects SV. However, SV can increase when there
is an increase in HR (during exercise for
example) when other mechanisms are activated, but when these
mechanisms fail, SV cannot be maintained during an elevated HR. These
mechanisms include increased venous return, venous constriction, increased
atrial and ventricular inotropy and enhanced rate of ventricular relaxation.
The ODM+ calculates SV by
multiplying the Stroke Distance (SD) by a constant accessed from the built-in
patient nomogram.
Normal values for a resting healthy
individual would be approximately 60-100mL. Patients undergoing surgery or in
critical illness situations may require higher than normal SV and it may be
more appropriate to aim for optimal rather than normal SV. See Stroke Volume Optimisation and Improved Outcomes.
Ventricular
stroke volume (SV) is often thought
of as the amount of blood (mL) ejected per beat by the left ventricle into the
aorta (or from the right ventricle into the pulmonary artery). This assumes,
however, that all the blood leaving the ventricle is ejected into the outflow
tract, but this is not the case when there is atrioventricular
valve regurgitation or an interventricular
septal defect. Therefore, a more precise definition for SV and one that is
used in echocardiography when assessing ventricular function is the difference
between the ventricular end-diastolic
volume (EDV) and the end-systolic
volume (ESV). The EDV is the filled volume of the ventricle before
contraction, and the ESV is the residual volume of blood remaining in the
ventricle after ejection. In a typical heart, the EDV is about 120 mL of blood
and the ESV is about 50 mL of blood. The difference in these two volumes, 70
mL, represents the SV (SV = EDV – ESV). Therefore, any
factor that alters either the EDV or the ESV will change the SV. For
example, an increase in EDV increases SV, whereas an increase in ESV decreases
SV.
There
are three primary mechanisms that regulate EDV and ESV, and therefore SV. These
are preload, afterload, and inotropy.
·
Preload
·
Inotropy
Stroke Volume Index (SVI) relates SV to
body surface area (BSA), thus relating heart performance to the size of the
individual. The unit of measurement is millilitres per square metre (ml/m2).
SVI = SV/BSA
Normal values for a resting
healthy individual would be approximately 35-65mL/m2. Patients undergoing
surgery or in critical illness situations may require higher than normal SVI
and it may be more appropriate to aim for optimal rather than normal SVI.
Cardiac Output (CO) is the amount of blood
the heart pumps from each ventricle per minute. It is usually expressed in
litres per minute (L/min).
CO = HR x SV
Changes in either HR or SV can alter CO.
Impaired regulation of SV (including preload, afterload and contractility) can have a significant
adverse affect on CO.
Normal values for a resting healthy
individual would be approximately 5-8L. Patients undergoing surgery or in
critical illness situations may require higher than normal CO and it may be
more appropriate to aim for optimal rather than normal CO.
Cardiac index (CI) is the cardiac output
proportional to the body surface area (BSA). The unit of measurement is
litres per minute per square metre (L/min/m2).
CI = CO x BSA
Normal values for a resting healthy
individual would be approximately 2.5-4.2L/m2. Patients undergoing surgery or
in critical illness situations may require higher than normal CI and it may be
more appropriate to aim for optimal rather than normal CI.
·
https://cvphysiology.com/cardiac-function/cf002
1.
Dvorak G.O., Hemodynamic Monitoring: Invasive and Non Invasive
Clinical Application. 2008 ed 4. Saunders.
2. Grossman S., and Porth C.M.,
Porth’s Pathophysiology: Concepts of Altered Health States. 2013 ed 9.
Lippincott Williams & Wilkins.
3. Klabunde R.E., Cardiovascular
Physiology Concepts. 2005. Lippincott Williams & Wilkins.
Published on 7 May 2024