10- Cardiac output, exercise and cardiac hypertrophy.

10- Cardiac output, exercise and cardiac hypertrophy.
Cardiac output: cardiac output is amount of blood pumped out of the heart each minute.
Cardiac output = Stroke volume x heart rate.
Stroke volume: It is the volume of blood ejected from the ventricle on each beat, is expressed by the following equation:
Stroke volume = End-diastolic volume - End-systolic volume.
Ejection fraction: It is the fraction of end-diastolic volume ejected in one beat. It is normally 55%. It is expressed by the following equation.
Ejection fraction = Stroke volume / End-diastolic volume.
Cardiac output (COP) is affected by body metabolism, exercise, age and size of the body. In young, healthy men, resting COP average about 5.6 L/minute. For women, this value is 10-20% less.
Cardiac index (CI):
Because there is a correlation between resting cardiac output (COP) and surface area of the body, it is important to find some mean by which COP of different sized people can be compared with one another. The COP is frequently stated in term of the cardiac index, which is the cardiac output /minute / m² of body surface. The normal average of cardiac index for adult is about 3.2 L.
The Cardiac index is rapidly rising from 2.5 L/minute/ m2 at infant to a level greater than 4 L/minute/m² at age 10 years, and then declines to about 2.4 L / minute / m² at age 80 years. See figure 31.

Figure (31): Correlation between CI and age (Guyton & Hall 2006).

The effect of various conditions on COP is summarized in table (5).
Table (5): The effect of various conditions on COP.
Causes that increase COP Causes that decrease COP Causes that no effect on COP
1-Anxiety and excitement Sitting or standing from lying position Sleep.
2- Eating Rapid arrhythmia Moderate change in environmental temperature
3-Exercise Heart disease
4- High environmental temperature.
5- Pregnancy.
6- Epinephrine

Methods of measurement of COP:
1-Direct Fick method:
Output of ventricle = O2 consumption (ml/minute) / A O2 – V O2.
= 250 ml /minute. / 190 ml/ L arterial blood – 140 ml/ L venous
blood in pulmonary artery.
= 250 ml/ minute / 50 ml/ L.
= 5L/minute.
Arterial O2 can be measured from sample taken from any artery in the systemic circulation as it has same O2 concentration, while venous O2 concentration is measured from pulmonary artery (by catheterization) because venous O2 concentration differ at different vein of systemic circulation.
2- Dilution method: Dye or a radioactive isotope of known volume and concentration is injected into an arm vein. The output of heart is equal to the indicator injected divided by its average concentration in arterial blood after a single circulation through heart.
3-Thermodilution method: The indicator used is cold saline. The saline is injected into the right atrium through catheter and temperature change in the blood is recorded in the pulmonary artery as right ventricular output is the same as left ventricular output. The temperature change is inversely proportionate to amount of blood flowing through the pulmonary artery. Cold saline is diluted by blood. This technique has two important advantages: 1- The saline is completely innocuous. 2- The cold is dissipated in tissue.
Factors controlling cardiac output: COP depends on two major factors:
1-Heart rat.
2- Stroke volume.
Stroke volume
A-Preload: It is the degree of myocardium to stretch before it contract according to Frank-Starling law. Preload depend on the end diastolic volume. Increase in end diastolic volume causes an increase in ventricle fibers length, which increase in contractility, that increase COP. End diastolic volume depend on the amount of blood return to the heart (venous return) which is the quantity of blood flowing from the veins into the right atrium. The venous return and the COP must be equal. Factors that decrease end-diastolic volume decrease COP.
B- After load: Normally the resistance in pulmonary circulation is low, while the resistance in systemic circulation is much higher. This why the pressure in systemic circulation is much higher than that of the pulmonary circulation. As the resistance increase ( such as in systemic hypertension) COP drops. See figure 32.

Figure (32): Correlation between COP and pressure (Guyton & Hall 2006).

By increasing the pressure for long period of time, cause hypertrophy of ventricular wall (concentric hypertrophy), in which increase in wall thickness but without increase in size of ventricle.
C-Myocardial contractility: It is the intrinsic ability of the cardiac muscle fibers to develop force at a given muscle length, also is called inotropism, can be estimated by the ejection fraction, which is normally 55%. When contractility increases, the ventricle can develop greater tension, pressure during systole and eject a large volume of blood than normal. Stroke volume increases as does ejection fraction, consequently
end systolic volume decreases.
Factors that causes increase contractility (positive inotropic effect) are:
1- Sympathetic stimulation exerts their inotropic effect via an action on cardiac ?1-adrenergic receptors.
2- Circulating catecholamine causes positive inotropic effect via B1 receptor.
3- Change in ionic concentration. Hyperkalemia decrease contractility, while hypercalcemia and hypernatremia increase contractility.
4- Cardiac rate. Myocardial contractility increases as heart rate increases because contractility correlates directly with intracellular Ca concentration.
5- Hormone. Thyroid hormone and glucagons which increase the formation of cAMP.
6- Cardiac rhythm. In ventricle extrasystole, the next contraction is stronger than the preceding normal contraction.
7- Xanthine, such as caffeine and theophylline that inhibit the breakdown of cAMP.
8- Digoxin, It has positive inotropic effect by inhibition of K-Na and Na-Ca ATPase in myocardium Intracellular Ca concentration increase and this increases the strength of contraction. Digoxin is the drug used in treatment of the heart failure.
Factors causes decrease contractility:
1- Myocardial infarction. 2- Myocarditis.
3- Hypercapnia, hypoxia and acidosis. 4- Parasympathetic stimulation.
COP increase during exercise by:
1- Sympathetic stimulation. 2- Increase catecholamine release.
3- Increase venous return. 4- Decrease after-load.
Graphical analysis of the normal function of left ventricle: Figure 33 shows the normal function of the left ventricle. It is divided into four phases:
1- Phase I (period of filling): it begin at a ventricular volume of about 70 ml (end-systolic volume) and the diastolic pressure near 0 mmHg. As blood flows into the ventricle from the left atrium, the ventricular volume normally increases to about 140 ml (end-diastolic volume). The volume increases of 70 ml. The ventricular pressure rising to about 5 mmHg. 2- Phase II (period of isovolumic contraction):
During this period the volume of ventricular blood does not change because all valves are closed. The pressure inside ventricle increase to pressure in the aorta (80 mmHg). 3- Phase III (period of ejection): During ejection the ventricular pressure rises because of still more contraction of the heart. At this time , the volume of ventricle decrease because aortic valve opens and blood flows out of ventricle into aorta.
4- Phase VI (period of isovolumic relaxation): it begins from end of ejection. The ventricular pressure decreases without any change in volume because aortic valve closes. The ventricle returns to its starting point.