Cardiac Output

Basics of Cardiac Output

• CO=HR X SV

• within the limit, an increase in HR will cause an increase in cardiac output (but decrease in SV)

• An abnormally high HR will cause decrease in both SV and CO

• High HR will drastically decrease ventricular filling time during diastolic period

• leading to drastic decrease in preload (blood volume in ventricle before ejection) and a decrease in SV and CO

Increase in CO During Exercise (Sympathetic Activation)

• sympathetic activation during exercise gives rise to positive inotropic effect to the contractile myocytes

• NE and Epi are potent B₁adrenergic agonist (increase HR and force of ventricular contraction)

• with a given HR and preload, an increase in force of contraction will lead to an increase in SV and subsequently leading to an increase in CO

Increase in CO During Exercise (Reduction in Peripheral Vascular Resistance)

• exercise causes vasoconstriction

• NE and Epi→ a₁adrenergic agonist (vasoconstriction)

• vasodilation is observed following vasoconstriction

• by vasodilators such as adenosine that are generated during transient ischemia

• CO and low pH also promote vasodilation

• process known as metabolic autoregulatory (reduction in vascular resistance within a contracting/working tissue)

• metabolic autoregulatory enhances blood perfusion to the working tissues

Increase in CO During Exercise (Enhance Venous Return)

• compression of skeletal muscles together with venous valves to enhance venous return

• when the skeletal muscles compress the veins, they force blood toward the heart (the skeletal muscle pump)

• valves in the veins prevent backflow of blood

Stroke Volume

• SV is the difference between the ventricular EDV (end diastolic volume) and the ESV (end systolic volume)

• EDV is volume of blood in left ventricle before ejection

• ESV is after ejection

• EDV=120, ESV=50, SV=70

Parameters That Affect SV (Increase Preload- Ventricular Compliance)

• compliance is defined as the change in volume divided by the change in pressure

Parameters That Affect SV (Increase Preload- Venous Return)

• increase in venous return will:

• stretch the myocytes

• increase force of contraction

• higher SV

• this mechanism is to ensure the outputs of both the ventricles are matched over time and to prevent the shifting of blood between pulmonary and systemic circulations

Parameters That Affect SV (Increase Preload- L-T relationship)

• the biophysical basis for the starlings law of the heart

• when the cardiac myocytes are stimulated with an increase in preload:

• active tension in the heart is increased

• increase in active tension will lead to an increase of force of contraction of the heart

• increase in force of contraction leads to increase in SV but not to ESV

Parameters That Affect SV (Afterload- Wall Stress)

• the ventricular wall tension developed during ventricular ejection

• the magnitude of wall tension developed is related to resistance, impedance, or pressure than the ventricle must overcome before blood can be ejected

• aortic pressure is one of the major components of afterload for the left ventricle

• Laplace’s Law:

• increase in wall thickness will reduce wall stress and reduce the afterload

Parameters That Affect SV (Contractility)

• define as the property of the contractile myocytes that account for the strength of contraction

• related to the intrinsic cellular mechanisms that regulate the interaction between actin and myosin

• independent of the preload and afterload

• a true indicator of inotropic state normally influenced by chemical or hormonal on the cardiac muscles

• increase in contractility will increase SV