Prof. Sultan Ayoub Meo MBBS, M.Phil, Ph.D (Pak), PG Dip Med Ed, M Med Ed (Scotland) FRCP (London), FRCP (Dublin), FRCP (Glasgow), FRCP (Edinburgh) Professor and Consultant, Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia STROKE VOLUME

LECTURE OUTLI NES / OBJECTIVES Understand the concept of preload and after-load Determine factors effecting the end-diastolic Volume Explain how cardiac contractility affect stroke volume Describe the pressure volume loop STUDENTS ABLE TO UNDERSTAND:

STROKE VOLUME The amount of blood pumped out of each ventricle per beat is called stroke volume (SV). 70 ml. The output of the heart per unit time (minute) is called cardiac output. Cardiac Out put= Stroke Volume x Hear Rate [70 mL x 72 beats / min= 5040 ml. Approx]  Cardiac Index: There is a correlation between resting cardiac output and body surface area. The output per minute per square meter of body surface is called cardiac index. Averages 3.2 L.

STROKE VOLUME SV = EDV - ESV Stroke volume is also defined as the difference between the ventricular End Diastolic Volume [EDV] and the End Systolic Volume [ ESV]. EDV is the filled volume of ventricle prior to contraction ESV is the residual volume of blood remaining in the ventricle after ejection. The EDV is about 120 ml of blood and the ESV about 50 ml of blood. The difference in these two volumes 70 ml represents the SV. Factor that alters either the EDV or the ESV will change SV. Example: Increase in EDV increases SV, whereas an increase in ESV decreases SV.

STROKE VOLUME When the heart contracts strongly, the end-systolic volume can be decreased to as little as 10 to 20 milliliters. Conversely, when large amounts of blood flow into the ventricles during diastole, the ventricular end diastolic volumes can become as great as 150 to 180 milliliters in healthy heart. By both increasing the end-diastolic volume and decreasing the end-systolic volume, the stroke volume output can be increased

STROKE VOLUME Preload affect the SV through the increase in venous return to the heart, increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers thereby increasing their preload. This leads to an increase in the force of ventricular contraction Afterload is related to the pressure that the ventricle generate to eject blood into the aorta. Changes in afterload affect the ability of the ventricle to eject blood and thereby alter ESV and SV. increase in afterload, increase aortic pressure, decreases SV, and causes ESV to increase.

STROKE VOLUME

STROKE VOLUME / CARDIAC OUT PUT Factor No change Sleep Moderate changes in environmental temperature IncreaseAnxiety and excitement (50–100%) Eating (30%) Exercise (up to 700%) High environmental temperature Pregnancy Epinephrine DecreaseSitting or standing from lying position (20–30%) Rapid arrhythmias, Heart disease

10 PRESSURE VOLUME LOOP

11 There are only three ways that the body regulates stroke volume from minute-to- minute: Filling pressure (preload) Aortic pressure (afterload) Contractility

12 The ejection loop PRESSURE VOLUME LOOP

13 Changing filling pressure changes stroke volume only by changing LVEDV This could be an example of transfusion Lowering LVEDP has the opposite effect (hemorrhage) PRESSURE VOLUME LOOP

14 Lowering the aortic pressure causes the ventricle to empty more completely. The stroke volume increases by an amount equal to the fall in LVESV. LVEDV is not affected. Raising aortic pressure has the opposite effect

15 Increasing contractility decreases LVESV and thus increases stroke volume. LVEDV is not affected. Heart failure has the opposite effect PRESSURE VOLUME LOOP

16 Decreasing the diastolic compliance decreases LVEDV and stroke volume but has no effect on LVESV PRESSURE VOLUME LOOP

17 The real ejection loop has a rounded top since the blood pressure increases during ejection (auxotonic beat)

18 Decreased compliance occurs only in disease and is not a physiological regulator

19 Dilation Hypertrophy Normal

20 Dilation Hypertrophy Normal Hypertrophy results from increased afterload over several months. Dilation results from persistently elevated preload over several days.

21 Dilation Hypertrophy Normal Hypertrophy results from increased afterload over several months. Dilation results from persistently elevated preload over several days. Fiber slippage at the desmosomes will occur before the fibers will extend beyond L o

22 Dilation Hypertrophy Normal Hypertrophy results from increased work load over several months. Increased mass Dilation results from persistently elevated preload over several days. Same mass The large chamber diameter and thin wall puts the dilated heart at a mechanical disadvantage.

23 Notice that stroke volume change in a reciprocal manner. Stroke Work = P x Vol As P goes up V naturally goes down so their product remains constant. Stroke work should be independent of any change in blood pressure.

24 If aortic pressure is held constant stroke volume increases with contractility. Stroke volume goes down as aortic pressure goes up. Since stroke volume changes reciprocally with aortic pressure their product (stroke work) is relatively independent of aortic pressure

25 How can we measure contractility in the patient? Ejection fraction = (LVEDV-LVESV) / LVEDV The fraction of the ventricular contents at end diastole that is ejected.

26 How can we measure contractility in the patient? Ejection fraction = (LVEDV-LVESV) / LVEDV A normal ejection fraction should be above Ejection fractions of are of concern. Values below 0.30 carry a poor prognosis.

27 How can we measure contractility in the patient? Ejection fraction = (LVEDV-LVESV) / LVEDV Can be easily measured by X-ray Nuclear techniques Echo normal concern <35 serious

28 Often contractility is lost in just a region of the heart as occurs in a myocardial infarction. Regional dysfunction can be seen with ultrasound or with a X-ray of the ventricle. NormalRegional akinesis