Heart muscle relies exclusively on aerobic metabolism for energy. Hypoxia an insufficient supply of oxygen leads to decreasing HRs, since metabolic reactions fueling heart contraction are restricted. Normal blood pH falls in the range of 7.
Recall that enzymes are the regulators or catalysts of virtually all biochemical reactions; they are sensitive to pH and will change shape slightly with values outside their normal range.
These variations in pH and accompanying slight physical changes to the active site on the enzyme decrease the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on HR.
Severe changes in pH will lead to denaturation of the enzyme. The last variable is body temperature. Elevated body temperature is called hyperthermia, and suppressed body temperature is called hypothermia. Slight hyperthermia results in increasing HR and strength of contraction. Hypothermia slows the rate and strength of heart contractions.
This distinct slowing of the heart is one component of the larger diving reflex that diverts blood to essential organs while submerged.
If sufficiently chilled, the heart will stop beating, a technique that may be employed during open heart surgery. Excessive hyperthermia and hypothermia will both result in death, as enzymes drive the body systems to cease normal function, beginning with the central nervous system.
Many of the same factors that regulate HR also impact cardiac function by altering SV. The three primary factors to consider are preload, or the stretch on the ventricles prior to contraction; the contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the resistance in the vessels.
These factors are summarized in Table Preload is the degree to which cardiac muscle cells are stretched from filling of the ventricles prior to contraction. Therefore preload is another way of expressing EDV. With increasing ventricular filling, both EDV or preload increase, and the cardiac muscle itself is stretched to a greater degree.
At rest, there is little stretch of the ventricular muscle, and the sarcomeres remain short. With increased ventricular filling, the ventricular muscle is increasingly stretched and the sarcomere length increases. As the sarcomeres reach their optimal lengths, they will contract more powerfully, because more of the myosin heads can bind to the actin on the thin filaments, forming cross bridges and increasing the strength of contraction and SV. If this process were to continue and the sarcomeres stretched beyond their optimal lengths, the force of contraction would decrease.
However, due to the physical constraints of the location of the heart, this excessive stretch is not a concern. One of the primary factors to consider is filling time , or the duration of ventricular diastole during which filling occurs.
The more rapidly the heart contracts, the shorter the filling time becomes, and the lower the EDV and preload are. This effect can be partially overcome by increasing the second variable, contractility, which raises the SV, but over time, the heart is unable to compensate for decreased filling time, and preload also decreases.
This principle states that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. This means that the greater the stretch of the ventricular muscle within limits , the more powerful the contraction is, which in turn increases SV.
Therefore, by increasing preload, you increase the second variable, contractility. Otto Frank — was a German physiologist; among his many published works are detailed studies of this important heart relationship. Ernest Starling — was an important English physiologist who also studied the heart. Any sympathetic stimulation to the venous system will increase venous return to the heart, which contributes to ventricular filling, and EDV and preload.
While much of the ventricular filling occurs while both atria and ventricles are in diastole, the contraction of the atria, the atrial kick refer to Figure 3, section It is virtually impossible to consider preload or ESV without including the concept of contractility. Indeed, the two parameters are intimately linked. Contractility refers to the force of the contraction of the heart muscle, which controls SV, and is the primary parameter for impacting ESV.
Not surprisingly, sympathetic stimulation is a positive inotrope, whereas parasympathetic stimulation is a negative inotrope. Sympathetic stimulation triggers the release of NE at the neuromuscular junction from the cardiac nerves and also stimulates the adrenal cortex to secrete epinephrine and NE.
In addition to their stimulatory effects on HR, they also bind to both alpha and beta receptors on the cardiac muscle cell membrane to increase metabolic rate and the force of contraction. This combination of actions has the net effect of increasing SV and leaving a smaller residual ESV in the ventricles. In comparison, parasympathetic stimulation releases ACh at the neuromuscular junction from the vagus nerve.
The membrane hyperpolarizes and decreases contraction to decrease the strength of contraction and SV, and to raise ESV. Since parasympathetic fibers are more widespread in the atria than in the ventricles, the primary site of action is in the upper chambers. Parasympathetic stimulation in the atria decreases the atrial kick and reduces EDV, which decreases ventricular stretch and preload, thereby further limiting the force of ventricular contraction.
Stronger parasympathetic stimulation also directly decreases the force of contraction of the ventricles. Several synthetic drugs, including dopamine and isoproterenol, have been developed that mimic the effects of epinephrine and NE by stimulating the influx of calcium ions from the extracellular fluid.
Higher concentrations of intracellular calcium ions increase the strength of contraction. Excess calcium hypercalcemia also acts as a positive inotropic agent.
The drug digitalis lowers HR and increases the strength of the contraction, acting as a positive inotropic agent by blocking the sequestering of calcium ions into the sarcoplasmic reticulum. This leads to higher intracellular calcium levels and greater strength of contraction. In addition to the catecholamines from the adrenal medulla, other hormones also demonstrate positive inotropic effects.
These include thyroid hormones and glucagon from the pancreas. 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 refers to the tension or force that the ventricles must develop to pump blood effectively against the resistance in the vascular system.
Any condition that increases resistance such as vasoconstiction or the disease atherosclerosis 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 as with vasodilation, decreases the afterload. 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.
Autonomic innervation and hormones largely regulate contractility. Contractility impacts EDV as does afterload. Skip to content Learning Objectives By the end of this section, you will be able to: Define cardiac output and explain how heart rate and stroke volume effect it Describe the effect of exercise on cardiac output Identify cardiovascular centers and cardiac reflexes that regulate heart function Describe factors affecting heart rate and force of contraction Explain the connection between preload, contractility, afterload and stroke volume Distinguish between positive and negative inotropic factors Summarize factors affecting stroke volume, heart rate and cardiac output.
Disorders of the…Heart: Abnormal Heart Rates. For an adult, normal resting HR will be in the range of 60— bpm. Bradycardia is the condition in which resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above bpm. Trained athletes typically have very low HRs.
If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant. However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues. The term relative bradycardia may be used with a patient who has a HR in the normal range but is still suffering from these symptoms.
Most patients remain asymptomatic as long as the HR remains above 50 bpm. For example, an increase in inotropy e. Conversely, a decrease in inotropy e. Therefore, while the primary effect of a change in preload, afterload or inotropy may be on either EDV or ESV, secondary changes can occur that can partially compensate for the initial change in SV.
For a more detailed description of these interactions, see the pages describing preload , afterload , or inotropy. Cardiovascular Physiology Concepts Richard E. Klabunde, PhD. Klabunde, all rights reserved Web Design by Jimp Studio. Heart rate HR also affects SV.
Changes in HR alone inversely affects SV. However, SV can increase when there is an increase in HR during exercise for example when other mechanisms are activated, but when these mechanisms fail, SV cannot be maintained during an elevated HR.
These mechanisms include increased venous return, venous constriction, increased atrial and ventricular inotropy and enhanced rate of ventricular relaxation. Normal values for a resting healthy individual would be approximately mL.
Patients undergoing surgery or in critical illness situations may require higher than normal SV and it may be more appropriate to aim for optimal rather than normal SV.
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