Afterload + Regulation of Heart Rate/Cardiac Output

Afterload: Amount of Back Pressure

Refers to the force that the ventricles must overcome in order to eject blood into their respective arteries; Determined by the blood pressure in the arteries in the pulmonary and systemic circuits

Increased Afterload

If afterload increases, ventricular pressure must increase to exceed pressure in the vessels and open the semilunar valves; Causes a decrease in stroke volume, which leads to a rise in the ESV of the ventricles

High Stroke Volume

High preload leads to a high EDV which stretches the muscle cells. High contractility causes a more forceful contraction which isn’t pumping against a lot of resistance; results in a high stroke volume

Low Stroke Volume

Low preload leads to a low EDV which reduces stretch of the muscle cells. Low contractility causes a less forceful contraction which is trying to pump against a lot of resistance; results in a low stroke volume

Ventricular Hypertrophy

Enlargement of the ventricles; associated with long-standing increases in afterload; Cardiac muscle cells need to generate more tension to continue pumping blood and they respond by making more myofibrils and getting bigger. However, this decreases the size of the heart lumen, leaving less space to fill with blood.

Right Ventricular Hypertrophy

Results from respiratory diseases or high blood pressure in the pulmonary circuit

Left Ventricular Hypertrophy

Results from high blood pressure in the systemic circuit

Chronotropic Agents

Factors that influence the rate at which the SA node depolarizes

Positive Chronotropic Agent

Anything that increases the rate at which the SA node fires; Sympathetic nervous system, certain hormones, elevated body temperature

Negative Chronotropic Agent

Anything that decreases the rate at which the SA node fires; Parasympathetic nervous system, decreased body temperature

Sympathetic Nerves

Stem from ganglia located along the spinal cord; neurons release norepinephrine which increases cardiac output with both positive chronotropic and inotropic effects; Increase heart rate by making SA node fire up to 180–200 or more times per minute; Cause more calcium ions to enter cardiac muscle cells, which increases contractility

Parasympathetic Nerves

Innervates the heart by the left and right vagus nerves; release acetylcholine; Affects the SA node primarily by decreasing the rate of action potential generation, although it also slows the rate of conduction through the AV node; Slows heart rate and can stop it temporarily if the stimulation is strong enough; Vagus nerves weakly reduce ventricular contractions due to their mild negative inotropic effects

Cardiac Regulation by the Endocrine System

Adrenal Medulla—Activated by the sympathetic nervous system to secrete Epinephrine and Norepinephrine; Positive inotropic and chronotropic agents, but their effects are longer-lasting; Thyroid Hormone and Glucagon have similar effects

Hormones That Influence Blood Volume and Preload

Aldosterone and Antidiuretic Hormone increase blood volume and preload by increasing water volume, and raise cardiac output; Atrial Natriuretic Peptide decreases blood volume and preload, reducing cardiac output