Cardiac Output and Venous Return

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. (7) myocarditis. (8) cardiac hypoxia.

Sympathetic stimulation can increase the effectiveness of the heart via:

(1) increasing the heart rate (2) increasing the strength of heart contraction.

Factors that cause hypereffective heart

(1) nervous stimulation and (2) hypertrophy of the heart muscle

Normal intraplural pressure is

-4 mmHg

What is the skeletal muscle pump?

Open venous valves permit flow of blood to heart. Contracted skeletal muscle closes valves to prevent backflow of blood

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.

stroke volume and cardiac output correlate directly with

end-diastolic volume, which correlates with venous return.

the greater the mean systemic filling pressure the easier it is for blood to

flow into the heart.

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

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.

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

factors affect cardiac output

metabolism, body size, exercise, age

Arterial and venous pressures come to equilibrium when all flow in the sys circulation ceases at 7 mmHg

not sure

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)

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

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.

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

The less the mean systemic filling pressure...

the more difficult it is for blood to flow into the heart.

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.

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

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

In the steady state, cardiac output equals

venous return.

Increasing intrapleural pressure will cause

an increase in atrial pressure by the same amount

Venous return is decreased when

atrial pressure rises nervous circulatory reflexes are absent

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.

Conditions which cause high CO and reduced TPR

beriberi, AV shunt, hyperthyroidism, anemia

Factors that alter intrapleural pressure and cardiac pressure

breathing against negative pressure, positive pressure breathing, cardiac tamponade,

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.

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

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.

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 decreased blood volume on cardiac output

decreases stressed volume and mean systemic pressure. cardiac output is decreased and right atrial pressure is decreased.

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. 6- Gravity.

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

What is the mean systemic filling pressure (Psf)?

7 mmHg

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

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

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.

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 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.