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Negative inotropic agents include hypoxia, acidosis, hyperkalemia, and a variety of synthetic drugs. These include numerous beta blockers and calcium channel blockers. Early beta blocker drugs include propranolol and pronethalol, and are credited with revolutionizing treatment of cardiac patients experiencing angina pectoris. There is also a large class of dihydropyridine, phenylalkylamine, and benzothiazepine calcium channel blockers that may be administered decreasing the strength of contraction and SV.

Afterload

Afterload refers to the tension that the ventricles must develop to pump blood effectively against the resistance in the vascular system. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood. Damage to the valves, such as stenosis, which makes them harder to open will also increase afterload. Any decrease in resistance decreases the afterload. [link] summarizes the major factors influencing SV, [link] summarizes the major factors influencing CO, and [link] and [link] summarize cardiac responses to increased and decreased blood flow and pressure in order to restore homeostasis.

Major factors influencing stroke volume

This table describes major factors influencing stroke volume. Preload may be raised due to fast filling time or increased venous return. These factors increase end diastolic volume and increase stroke volume. Preload may be lowered due to decreased thyroid hormones, decreased calcium ions, high or low potassium ions, high or low sodium, low body temperature, hypoxia, abnormal pH balance, or drugs (for example, calcium channel blockers). These factors decrease end diastolic volume and decrease stroke volume. Contractility may be raised due to sympathetic stimulation, epinephrine and norepinephrine, high intracellular calcium ions, high blood calcium level, thyroid hormones, or glucagon. These factors decrease end systolic volume and increase stroke volume. Contractility may be lowered due to parasympathetic stimulation, acetylcholine, hypoxia, or hyperkalemia. These factors increase end systolic volume and decrease stroke volume. Afterload may be raised due to increased vascular resistance or semilunar valve damage. These factors increase end systolic volume and decrease stroke volume. Afterload may be lowered due to decreased vascular resistance. This factor decreases end systolic volume and increases stroke volume.
Multiple factors impact preload, afterload, and contractility, and are the major considerations influencing SV.

Summary of major factors influencing cardiac output

This flowchart lists all the important factors that affect cardiac output.
The primary factors influencing HR include autonomic innervation plus endocrine control. Not shown are environmental factors, such as electrolytes, metabolic products, and temperature. The primary factors controlling SV include preload, contractility, and afterload. Other factors such as electrolytes may be classified as either positive or negative inotropic agents.
Cardiac Response to Decreasing Blood Flow and Pressure Due to Decreasing Cardiac Output
Baroreceptors (aorta, carotid arteries, venae cavae, and atria) Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive to Decreasing stretch Decreasing O 2 and increasing CO 2 , H + , and lactic acid
Target Parasympathetic stimulation suppressed Sympathetic stimulation increased
Response of heart Increasing heart rate and increasing stroke volume Increasing heart rate and increasing stroke volume
Overall effect Increasing blood flow and pressure due to increasing cardiac output; hemostasis restored Increasing blood flow and pressure due to increasing cardiac output; hemostasis restored
Cardiac Response to Increasing Blood Flow and Pressure Due to Increasing Cardiac Output
Baroreceptors (aorta, carotid arteries, venae cavae, and atria) Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive to Increasing stretch Increasing O 2 and decreasing CO 2 , H + , and lactic acid
Target Parasympathetic stimulation increased Sympathetic stimulation suppressed
Response of heart Decreasing heart rate and decreasing stroke volume Decreasing heart rate and decreasing stroke volume
Overall effect Decreasing blood flow and pressure due to decreasing cardiac output; hemostasis restored Decreasing blood flow and pressure due to decreasing cardiac output; hemostasis restored

Chapter review

Many factors affect HR and SV, and together, they contribute to cardiac function. HR is largely determined and regulated by autonomic stimulation and hormones. There are several feedback loops that contribute to maintaining homeostasis dependent upon activity levels, such as the atrial reflex, which is determined by venous return.

SV is regulated by autonomic innervation and hormones, but also by filling time and venous return. Venous return is determined by activity of the skeletal muscles, blood volume, and changes in peripheral circulation. Venous return determines preload and the atrial reflex. Filling time directly related to HR also determines preload. Preload then impacts both EDV and ESV. Autonomic innervation and hormones largely regulate contractility. Contractility impacts EDV as does afterload. CO is the product of HR multiplied by SV. SV is the difference between EDV and ESV.

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Source:  OpenStax, Anatomy & Physiology. OpenStax CNX. Feb 04, 2016 Download for free at http://legacy.cnx.org/content/col11496/1.8
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