Stroke Volume

Stroke volume is governed by three factors called preload, contractility, and afterload. Increased preload or contractility increases stroke volume, while increased afterload opposes the emptying of the ventricles and reduces stroke volume.

Preload

The amount of tension in the ventricular myocardium immediately before it begins to contract is called the preload. To understand how it influences stroke volume, imagine yourself engaged in heavy exercise. As active muscles massage your veins, they drive more blood back to your heart, increasing venous return. As more blood enters your heart, it stretches the myocardium. Due to the length-tension relationship of striated muscle explained in chapter 11, moderate stretch enables the myocytes to generate more tension when they begin to contract—that is, it increases the preload. If the ventricles contract more forcefully, they expel more blood, thus adjusting your cardiac output to the increase in venous return.

This theory is summarized by the Frank-Starling law of the heart.32 In a concise, symbolic way, it states that SV « EDV. In other words, the ventricles tend to eject as much blood as they receive. Within limits, the more they are stretched, the harder they contract when stimulated.

While relaxed skeletal muscle is normally at an optimum length for the most forceful contraction, relaxed cardiac muscle is at less than optimum length. Additional stretch therefore produces a significant increase in contraction force on the next beat. This helps balance the output of the two ventricles. For example, if the right ventricle begins to pump an increased amount of blood, this soon arrives at the left ventricle, stretches it more than before, and causes it to increase its stroke volume to match that of the right.

Contractility

The contractility of the myocardium refers to its contraction force for a given preload. It does not describe an

32Otto Frank (1865-1944), German physiologist; Ernest Henry Starling

(1866-1927), English physiologist

Saladin: Anatomy & I 19. The Circulatory System: I Text

Physiology: The Unity of The Heart Form and Function, Third Edition

740 Part Four Regulation and Maintenance increase in tension resulting from increased stretch but rather an increase caused by factors that make the myocytes more responsive to stimulation. Factors that increase contractility are called positive inotropic33 agents, and those that reduce it are negative inotropic agents.

Remember that Ca2+ is essential to the excitation-contraction coupling of muscle and prolongs the plateau of the myocardial action potential. Calcium therefore has a positive inotropic effect, as do agents that increase its availability to the myofilaments. Epinephrine and norepinephrine act through cAMP to open Ca2+ channels. By increasing the supply of Ca2+ to the myofilaments, they have a positive inotropic effect. Glucagon acts by stimulating the formation of cAMP; a solution of glucagon and calcium chloride is sometimes used for the emergency treatment of heart attacks. Digitalis, a cardiac stimulant from the foxglove plant, is used to treat congestive heart failure. It acts indirectly by inhibiting the Na+-K+ pumps of the myocardium, raising intracellular Na+ concentration, and increasing the amount of Ca2+ in the sarcoplasm. Hypercalcemia causes more than the usual amount of Ca2+ to diffuse into the sarcoplasm and thus produces strong, prolonged contractions. In extreme cases, it can cause cardiac arrest in systole. Hypocalcemia can cause a weak, irregular heartbeat and potentially cause diastolic arrest. However, as explained in chapter 8, severe hypocal-cemia is likely to kill through skeletal muscle paralysis and suffocation before the cardiac effects are felt.

I_ The vagus nerves have a negative inotropic effect on the atria, but they provide so little innervation to the ven-p tricular myocytes that they have little effect on the ventri-r cles. Hyperkalemia has a negative inotropic effect because it ^bkJ reduces the strength of myocardial action potentials and thus reduces the release of Ca2+ into the sarcoplasm. The heart becomes dilated and flaccid. Hypokalemia, however, has little effect on contractility. There are other chronotropic and inotropic agents too numerous to mention here. The ones we have discussed are summarized in table 19.2.

_Think About It_

Suppose a person has a heart rate of 70 bpm and a stroke volume of 70 mL. A negative inotropic agent then reduces the stroke volume to 50 mL. What would the new heart rate have to be to maintain the same cardiac output?

Afterload

The blood pressure in the arteries just outside the semilunar valves, called the afterload, opposes the opening of these valves. An increased afterload therefore reduces

Table 19.2 Some Chronotropic and Inotropic Agents

Chronotropic Agents

Positive

Negative

Sympathetic stimulation Epinephrine and norepinephrine Thyroid hormone Hypocalcemia Hypercapnia and acidosis Digitalis

Parasympathetic stimulation

Acetylcholine

Hyperkalemia

Hypokalemia

Hypercalcemia

Hypoxia

Inotropic Agents

Positive

Negative

Sympathetic stimulation

Epinephrine and norepinephrine

Hypercalcemia

Digitalis

Glucagon

(Parasympathetic effect negligible)

Hyperkalemia

Hypocalcemia

Myocardial hypoxia

Myocardial hypercapnia

stroke volume. Anything that impedes arterial circulation can increase the afterload. For example, in some lung diseases, scar tissue forms in the lungs and restricts pulmonary circulation. This increases the afterload in the pulmonary trunk and opposes emptying of the right ventricle. As the ventricle works harder to overcome this resistance, it gets larger like any other muscle. Stress and hypertrophy of a ventricle can eventually cause it to weaken and fail. Right ventricular failure due to obstructed pulmonary circulation is called cor pulmonale34 (CORE PUL-mo-NAY-lee). It is a common complication of emphysema, chronic bronchitis, and black lung disease (see chapter 22).

Was this article helpful?

0 0
Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

Get My Free Ebook


Post a comment