Frank Starling Mechanism of the heart
the greater the heart muscle is stretched during filling, the greater is the force of contraction and greater the quantity of blood pumped into the aorta. Within physiological limits, the heart pumps all the blood that returns to it by the way of the veins.
What explains the Frank Starling Mechanism?
Extra blood flows into ventricles, cardiac muscle stretched greater length causes muscle to contract with more force (actin and myosin filaments at a more optimal degree of overlap for force). Also, stretching of right atrium increases the heart rate by 10-20 per cent.
Frank-Starling relationship, states that the volume of blood ejected by the ventricle depends on
the volume present in the ventricle at the end of diastole.
The volume present at the end of diastole, in turn, depends on
the volume returned to the heart, or the venous return.
stroke volume and cardiac output correlate directly with
end-diastolic volume, which correlates with venous return.
Factors that cause hypereffective heart
(1) nervous stimulation and
(2) hypertrophy of the heart muscle
Sympathetic stimulation can increase the effectiveness of the heart via:
(1) increasing the heart rate
(2) increasing the strength of heart contraction.
Factors that can cause a hypoeffective heart:
(1) coronary artery blockage.
(2) inhibition of nervous excitation of the heart.
(3) abonrmal heart rhythm.
(4) valvular heart disease.
(5) increased arterial pressure.
(6) congenital heart disease.
(8) cardiac hypoxia.
Dinitrophenol given with an intact nervous system will cause
vasodilation and increased CO and venous return but stable arterial pressure
Dinitrophenol given without an intact nervous system will cause
vasodilation and slight increase in CO and venous return but an extreme increase in arterial pressure
What is the effect of exercise on arterial pressure?
Exercise causes peripheral vasodilation but causes vasoconstriction in the larger veins = increased cardiac contractility, increased HR which = increased pressure - forcing more blood flow to muscles
Two groups of conditions that cause abnormally low cardiac output:
1-Decreased cardiac output caused by cardiac factors (severe coronary blockage and MI, valvular disease, cardiac tamponade
2-Decreased CO caused by non-cardiac peripheral factors- decreased VR: blood loss, acute venous dilation w/ no symp nervous system, obstruction of lg vein, decreased tissue mass
Factors that alter intrapleural pressure and cardiac pressure
breathing against negative pressure, positive pressure breathing, cardiac tamponade,
Three factors affect venous return
right atrial pressure (backward force on veins)
degree of filling of systemic circulation (force of systemic blood toward heart)
resistance to blood flow (between peripheral and right atrium)
Why does atrial pressure increase reduce venous return so drastically?
Any increase in back pressure causes the blood to dam up so there is no venous return = venous stasis. Pumping by the heart also falls to zero because of decreasing venous return
Arterial and venous pressures come to equilibrium when all flow in the sys circulation ceases at 7 mmHg
Plateau in the venous return curve at negative atrial pressure and continued decrease in pressure is caused by
collapse of the veins in the chest
The value for right atrial pressure at which venous return is zero is called
the mean systemic pressure. This is the pressure that would be measured throughout the cardiovascular system if the heart was stopped
Effect of blood volume 0-4L on mean circulatory filling pressure
When the blood volume ranges from 0 to 4 L, all of the blood will be in the unstressed volume (the veins), producing no pressure, and the mean systemic pressure will be zero.
Effect of blood volume >4L on mean circulatory filling pressure
When blood volume is greater than 4 L, some of the blood will be in the stressed volume (the arteries) and produce pressure.
Effect of sympathetic stimulation on mean systemic filling pressure
sympathetic stimulation causes blood to hold less bloos and push it to the stressed volume and increases mean sys filling pressure to increase
Effect of sympathetic inhibition on mean systemic filling pressure
veins hold more blood, decrease in stressed volume, increase in unstressed volume and decrease in systemic filling pressure
The less the mean systemic filling pressure...
the more difficult it is for blood to flow into the heart.
The effect of TPR on venous return : A decrease in TPR...
TPR makes it easier for blood to flow from the arterial to the venous side of the circulation and back to the heart.
The effect of TPR on venous return: An increase in TPR
makes it more difficult for blood to flow from the arterial to the venous side of the circulation and back to the heart
Effect of a sympathetic stimulation (such as a positive inotropic agent like digitalis) on CO
cardiac output is increased and right atrial pressure is decreased.
Effect of a sympathetic inhibition (such as a negative inotropic agent) on CO
decrease in contractility and a decrease in cardiac output increase in atrial pressure
Effect of increased blood volume on cardiac output
increase the stressed volume, increase the mean systemic pressure, cardiac output is increased and right atrial pressure is increased
Effect of decreased blood volume on cardiac output
decreases stressed volume and mean systemic pressure. cardiac output is decreased and right atrial pressure is decreased.
Increased CO from transfusion lasts for only a few minutes. This is because capillary pressure
increases so that fluid begins to transude out of the capillaries into the tissues, thereby returning the blood volume toward normal.
Increased CO from transfusion lasts for only a few minutes. This is because increased pressure in the veins causes the veins to
continue distending by the mechanism called stress-relaxation, thus reducing the mean systemic pressure.
Increased CO from transfusion lasts for only a few minutes. This is because excess blood flow causes
autoregulatory increase in peripheral resistance, thus increasing the resistance to venous return.
What are the factors that control venous return?
1- Skeletal muscle pump.
2- Respiratory pump (↑ in inspiration ).
3- Blood volume.
4- Pressure gradient.
5- Venous pressure.