Module 14: The Cardiovascular System: The Heart

Lesson 7: Cardiac Output: Factors Influencing Heart Rate

Cung Lượng Tim: Yếu Tố Ảnh Hưởng Đến Nhịp Tim

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Dưới đây là danh sách những thuật ngữ Y khoa của module The Cardiovascular System: The Heart.
Khái quát được số lượng thuật ngữ sẽ xuất hiện trong bài đọc và nghe sẽ giúp bạn thoải mái tiêu thụ nội dung hơn. Sau khi hoàn thành nội dung đọc và nghe, bạn hãy quay lại đây và luyện tập (practice) để quen dần các thuật ngữ này. Đừng ép bản thân phải nhớ các thuật ngữ này vội vì bạn sẽ gặp và ôn lại danh sách này trong những bài học (lesson) khác của cùng một module.

Medical Terminology: The Cardiovascular System: The Heart

afterload
force the ventricles must develop to effectively pump blood against the resistance in the vessels
anastomosis
(plural = anastomoses) area where vessels unite to allow blood to circulate even if there may be partial blockage in another branch
anterior cardiac veins
vessels that parallel the small cardiac arteries and drain the anterior surface of the right ventricle; bypass the coronary sinus and drain directly into the right atrium
anterior interventricular artery
(also, left anterior descending artery or LAD) major branch of the left coronary artery that follows the anterior interventricular sulcus
anterior interventricular sulcus
sulcus located between the left and right ventricles on the anterior surface of the heart
aortic valve
(also, aortic semilunar valve) valve located at the base of the aorta
artificial pacemaker
medical device that transmits electrical signals to the heart to ensure that it contracts and pumps blood to the body
atrial reflex
(also, called Bainbridge reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases
atrioventricular (AV) node
clump of myocardial cells located in the inferior portion of the right atrium within the atrioventricular septum; receives the impulse from the SA node, pauses, and then transmits it into specialized conducting cells within the interventricular septum
atrioventricular bundle
(also, bundle of His) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches
atrioventricular bundle branches
(also, left or right bundle branches) specialized myocardial conductile cells that arise from the bifurcation of the atrioventricular bundle and pass through the interventricular septum; lead to the Purkinje fibers and also to the right papillary muscle via the moderator band
atrioventricular septum
cardiac septum located between the atria and ventricles; atrioventricular valves are located here
atrioventricular valves
one-way valves located between the atria and ventricles; the valve on the right is called the tricuspid valve, and the one on the left is the mitral or bicuspid valve
atrium
(plural = atria) upper or receiving chamber of the heart that pumps blood into the lower chambers just prior to their contraction; the right atrium receives blood from the systemic circuit that flows into the right ventricle; the left atrium receives blood from the pulmonary circuit that flows into the left ventricle
auricle
extension of an atrium visible on the superior surface of the heart
autonomic tone
contractile state during resting cardiac activity produced by mild sympathetic and parasympathetic stimulation
autorhythmicity
ability of cardiac muscle to initiate its own electrical impulse that triggers the mechanical contraction that pumps blood at a fixed pace without nervous or endocrine control
Bachmann’s bundle
(also, interatrial band) group of specialized conducting cells that transmit the impulse directly from the SA node in the right atrium to the left atrium
Bainbridge reflex
(also, called atrial reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases
baroreceptor reflex
autonomic reflex in which the cardiac centers monitor signals from the baroreceptor stretch receptors and regulate heart function based on blood flow
bicuspid valve
(also, mitral valve or left atrioventricular valve) valve located between the left atrium and ventricle; consists of two flaps of tissue
bulbus cordis
portion of the primitive heart tube that will eventually develop into the right ventricle
bundle of His
(also, atrioventricular bundle) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches
cardiac cycle
period of time between the onset of atrial contraction (atrial systole) and ventricular relaxation (ventricular diastole)
cardiac notch
depression in the medial surface of the superior lobe of the left lung where the apex of the heart is located
cardiac output (CO)
amount of blood pumped by each ventricle during one minute; equals HR multiplied by SV
cardiac plexus
paired complex network of nerve fibers near the base of the heart that receive sympathetic and parasympathetic stimulations to regulate HR
cardiac reflexes
series of autonomic reflexes that enable the cardiovascular centers to regulate heart function based upon sensory information from a variety of visceral sensors
cardiac reserve
difference between maximum and resting CO
cardiac skeleton
(also, skeleton of the heart) reinforced connective tissue located within the atrioventricular septum; includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta; the point of attachment for the heart valves
cardiogenic area
area near the head of the embryo where the heart begins to develop 18–19 days after fertilization
cardiogenic cords
two strands of tissue that form within the cardiogenic area
cardiomyocyte
muscle cell of the heart
chordae tendineae
string-like extensions of tough connective tissue that extend from the flaps of the atrioventricular valves to the papillary muscles
circumflex artery
branch of the left coronary artery that follows coronary sulcus
coronary arteries
branches of the ascending aorta that supply blood to the heart; the left coronary artery feeds the left side of the heart, the left atrium and ventricle, and the interventricular septum; the right coronary artery feeds the right atrium, portions of both ventricles, and the heart conduction system
coronary sinus
large, thin-walled vein on the posterior surface of the heart that lies within the atrioventricular sulcus and drains the heart myocardium directly into the right atrium
coronary sulcus
sulcus that marks the boundary between the atria and ventricles
coronary veins
vessels that drain the heart and generally parallel the large surface arteries
diastole
period of time when the heart muscle is relaxed and the chambers fill with blood
ejection fraction
portion of the blood that is pumped or ejected from the heart with each contraction; mathematically represented by SV divided by EDV
electrocardiogram (ECG)
surface recording of the electrical activity of the heart that can be used for diagnosis of irregular heart function; also abbreviated as EKG
end diastolic volume (EDV)
(also, preload) the amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction
end systolic volume (ESV)
amount of blood remaining in each ventricle following systole
endocardial tubes
stage in which lumens form within the expanding cardiogenic cords, forming hollow structures
endocardium
innermost layer of the heart lining the heart chambers and heart valves; composed of endothelium reinforced with a thin layer of connective tissue that binds to the myocardium
endothelium
layer of smooth, simple squamous epithelium that lines the endocardium and blood vessels
epicardial coronary arteries
surface arteries of the heart that generally follow the sulci
epicardium
innermost layer of the serous pericardium and the outermost layer of the heart wall
filling time
duration of ventricular diastole during which filling occurs
foramen ovale
opening in the fetal heart that allows blood to flow directly from the right atrium to the left atrium, bypassing the fetal pulmonary circuit
fossa ovalis
oval-shaped depression in the interatrial septum that marks the former location of the foramen ovale
Frank-Starling mechanism
relationship between ventricular stretch and contraction in which the force of heart contraction is directly proportional to the initial length of the muscle fiber
great cardiac vein
vessel that follows the interventricular sulcus on the anterior surface of the heart and flows along the coronary sulcus into the coronary sinus on the posterior surface; parallels the anterior interventricular artery and drains the areas supplied by this vessel
heart block
interruption in the normal conduction pathway
heart bulge
prominent feature on the anterior surface of the heart, reflecting early cardiac development
heart rate (HR)
number of times the heart contracts (beats) per minute
heart sounds
sounds heard via auscultation with a stethoscope of the closing of the atrioventricular valves (“lub”) and semilunar valves (“dub”)
hypertrophic cardiomyopathy
pathological enlargement of the heart, generally for no known reason
inferior vena cava
large systemic vein that returns blood to the heart from the inferior portion of the body
interatrial band
(also, Bachmann’s bundle) group of specialized conducting cells that transmit the impulse directly from the SA node in the right atrium to the left atrium
interatrial septum
cardiac septum located between the two atria; contains the fossa ovalis after birth
intercalated disc
physical junction between adjacent cardiac muscle cells; consisting of desmosomes, specialized linking proteoglycans, and gap junctions that allow passage of ions between the two cells
internodal pathways
specialized conductile cells within the atria that transmit the impulse from the SA node throughout the myocardial cells of the atrium and to the AV node
interventricular septum
cardiac septum located between the two ventricles
isovolumic contraction
(also, isovolumetric contraction) initial phase of ventricular contraction in which tension and pressure in the ventricle increase, but no blood is pumped or ejected from the heart
isovolumic ventricular relaxation phase
initial phase of the ventricular diastole when pressure in the ventricles drops below pressure in the two major arteries, the pulmonary trunk, and the aorta, and blood attempts to flow back into the ventricles, producing the dicrotic notch of the ECG and closing the two semilunar valves
left atrioventricular valve
(also, mitral valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue
marginal arteries
branches of the right coronary artery that supply blood to the superficial portions of the right ventricle
mesoderm
one of the three primary germ layers that differentiate early in embryonic development
mesothelium
simple squamous epithelial portion of serous membranes, such as the superficial portion of the epicardium (the visceral pericardium) and the deepest portion of the pericardium (the parietal pericardium)
middle cardiac vein
vessel that parallels and drains the areas supplied by the posterior interventricular artery; drains into the great cardiac vein
mitral valve
(also, left atrioventricular valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue
moderator band
band of myocardium covered by endocardium that arises from the inferior portion of the interventricular septum in the right ventricle and crosses to the anterior papillary muscle; contains conductile fibers that carry electrical signals followed by contraction of the heart
murmur
unusual heart sound detected by auscultation; typically related to septal or valve defects
myocardial conducting cells
specialized cells that transmit electrical impulses throughout the heart and trigger contraction by the myocardial contractile cells
myocardial contractile cells
bulk of the cardiac muscle cells in the atria and ventricles that conduct impulses and contract to propel blood
myocardium
thickest layer of the heart composed of cardiac muscle cells built upon a framework of primarily collagenous fibers and blood vessels that supply it and the nervous fibers that help to regulate it
negative inotropic factors
factors that negatively impact or lower heart contractility
P wave
component of the electrocardiogram that represents the depolarization of the atria
pacemaker
cluster of specialized myocardial cells known as the SA node that initiates the sinus rhythm
papillary muscle
extension of the myocardium in the ventricles to which the chordae tendineae attach
pectinate muscles
muscular ridges seen on the anterior surface of the right atrium
pericardial cavity
cavity surrounding the heart filled with a lubricating serous fluid that reduces friction as the heart contracts
pericardial sac
(also, pericardium) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium
pericardium
(also, pericardial sac) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium
positive inotropic factors
factors that positively impact or increase heart contractility
posterior cardiac vein
vessel that parallels and drains the areas supplied by the marginal artery branch of the circumflex artery; drains into the great cardiac vein
posterior interventricular artery
(also, posterior descending artery) branch of the right coronary artery that runs along the posterior portion of the interventricular sulcus toward the apex of the heart and gives rise to branches that supply the interventricular septum and portions of both ventricles
posterior interventricular sulcus
sulcus located between the left and right ventricles on the posterior surface of the heart
preload
(also, end diastolic volume) amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction
prepotential depolarization
(also, spontaneous depolarization) mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise
primitive atrium
portion of the primitive heart tube that eventually becomes the anterior portions of both the right and left atria, and the two auricles
primitive heart tube
singular tubular structure that forms from the fusion of the two endocardial tubes
primitive ventricle
portion of the primitive heart tube that eventually forms the left ventricle
pulmonary arteries
left and right branches of the pulmonary trunk that carry deoxygenated blood from the heart to each of the lungs
pulmonary capillaries
capillaries surrounding the alveoli of the lungs where gas exchange occurs: carbon dioxide exits the blood and oxygen enters
pulmonary circuit
blood flow to and from the lungs
pulmonary trunk
large arterial vessel that carries blood ejected from the right ventricle; divides into the left and right pulmonary arteries
pulmonary valve
(also, pulmonary semilunar valve, the pulmonic valve, or the right semilunar valve) valve at the base of the pulmonary trunk that prevents backflow of blood into the right ventricle; consists of three flaps
pulmonary veins
veins that carry highly oxygenated blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and to the many branches of the systemic circuit
Purkinje fibers
specialized myocardial conduction fibers that arise from the bundle branches and spread the impulse to the myocardial contraction fibers of the ventricles
QRS complex
component of the electrocardiogram that represents the depolarization of the ventricles and includes, as a component, the repolarization of the atria
right atrioventricular valve
(also, tricuspid valve) valve located between the right atrium and ventricle; consists of three flaps of tissue
semilunar valves
valves located at the base of the pulmonary trunk and at the base of the aorta
septum
(plural = septa) walls or partitions that divide the heart into chambers
septum primum
flap of tissue in the fetus that covers the foramen ovale within a few seconds after birth
sinoatrial (SA) node
known as the pacemaker, a specialized clump of myocardial conducting cells located in the superior portion of the right atrium that has the highest inherent rate of depolarization that then spreads throughout the heart
sinus rhythm
normal contractile pattern of the heart
sinus venosus
develops into the posterior portion of the right atrium, the SA node, and the coronary sinus
small cardiac vein
parallels the right coronary artery and drains blood from the posterior surfaces of the right atrium and ventricle; drains into the coronary sinus, middle cardiac vein, or right atrium
spontaneous depolarization
(also, prepotential depolarization) the mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise
stroke volume (SV)
amount of blood pumped by each ventricle per contraction; also, the difference between EDV and ESV
sulcus
(plural = sulci) fat-filled groove visible on the surface of the heart; coronary vessels are also located in these areas
superior vena cava
large systemic vein that returns blood to the heart from the superior portion of the body
systemic circuit
blood flow to and from virtually all of the tissues of the body
systole
period of time when the heart muscle is contracting
T wave
component of the electrocardiogram that represents the repolarization of the ventricles
target heart rate
range in which both the heart and lungs receive the maximum benefit from an aerobic workout
trabeculae carneae
ridges of muscle covered by endocardium located in the ventricles
tricuspid valve
term used most often in clinical settings for the right atrioventricular valve
truncus arteriosus
portion of the primitive heart that will eventually divide and give rise to the ascending aorta and pulmonary trunk
valve
in the cardiovascular system, a specialized structure located within the heart or vessels that ensures one-way flow of blood
ventricle
one of the primary pumping chambers of the heart located in the lower portion of the heart; the left ventricle is the major pumping chamber on the lower left side of the heart that ejects blood into the systemic circuit via the aorta and receives blood from the left atrium; the right ventricle is the major pumping chamber on the lower right side of the heart that ejects blood into the pulmonary circuit via the pulmonary trunk and receives blood from the right atrium
ventricular ejection phase
second phase of ventricular systole during which blood is pumped from the ventricle
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The autorhythmicity inherent in cardiac cells keeps the heart beating at a regular pace; however, the heart is regulated by and responds to outside influences as well. Neural and endocrine controls are vital to the regulation of cardiac function. In addition, the heart is sensitive to several environmental factors, including electrolytes.
HRs vary considerably, not only with exercise and fitness levels, but also with age. Newborn resting HRs may be 120 bpm. HR gradually decreases until young adulthood and then gradually increases again with age.

Maximum HRs are normally in the range of 200–220 bpm, although there are some extreme cases in which they may reach higher levels. As one ages, the ability to generate maximum rates decreases. This may be estimated by taking the maximal value of 220 bpm and subtracting the individual’s age. So a 40-year-old individual would be expected to hit a maximum rate of approximately 180, and a 60-year-old person would achieve a HR of 160.
Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high. However, as HR continues to increase, SV gradually decreases due to decreased filling time. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV. Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately 120 bpm, CO will rise. As HR increases from 120 to 160 bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. As HR continues to rise above 160 bpm, CO actually decreases as SV falls faster than HR increases. So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between 120 and 160 bpm, so CO is maintained. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age.
Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata (Figure 1). The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm.

Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart. The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (NE) at the neuromuscular junction of the cardiac nerves. NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. It opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.

NE binds to the beta-1 receptor. Some cardiac medications (for example, beta blockers) work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. Overprescription of these drugs may lead to bradycardia and even stoppage of the heart.

Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one’s foot from the break and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require sympathetic stimulation. Figure 2 illustrates the effects of parasympathetic and sympathetic stimulation on the normal sinus rhythm.
The cardiovascular center receives input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system. Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. Any such increase in physical activity would logically warrant increased blood flow. The cardiac centers monitor these increased rates of firing, and suppress parasympathetic stimulation and increase sympathetic stimulation as needed in order to increase blood flow.

Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.

There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is also true.

Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid, plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves. These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood flow, based on the relative levels of these substances.

The limbic system can also significantly impact HR related to emotional state. During periods of stress, it is not unusual to identify higher than normal HRs, often accompanied by a surge in the stress hormone cortisol. Individuals experiencing extreme anxiety may manifest panic attacks with symptoms that resemble those of heart attacks. These events are typically transient and treatable. Meditation techniques have been developed to ease anxiety and have been shown to lower HR effectively. Doing simple deep and slow breathing exercises with one’s eyes closed can also significantly reduce this anxiety and HR.
Using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over HR. However, there are a number of other factors that have an impact on HR as well, including epinephrine, NE, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance (Table 1 and Table 2). After reading this section, the importance of maintaining homeostasis should become even more apparent.

A. Epinephrine and Norepinephrine

The catecholamines, epinephrine and NE, secreted by the adrenal medulla form one component of the extended fight-or-flight mechanism. The other component is sympathetic stimulation. Epinephrine and NE have similar effects: binding to the beta-1 receptors, and opening sodium and calcium ion chemical- or ligand-gated channels. The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization is shortened. However, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. There is no parasympathetic stimulation to the adrenal medulla.

B. Thyroid Hormones

In general, increased levels of thyroid hormone, or thyroxin, increase cardiac rate and contractility. The impact of thyroid hormone is typically of a much longer duration than that of the catecholamines. The physiologically active form of thyroid hormone, T3 or triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. It also impacts the beta adrenergic response similar to epinephrine and NE described above. Excessive levels of thyroxin may trigger tachycardia.

C. Calcium

Calcium ion levels have great impacts upon both HR and contractility; as the levels of calcium ions increase, so do HR and contractility. High levels of calcium ions (hypercalcemia) may be implicated in a short QT interval and a widened T wave in the ECG. The QT interval represents the time from the start of depolarization to repolarization of the ventricles, and includes the period of ventricular systole. Extremely high levels of calcium may induce cardiac arrest. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions.

D. Caffeine and Nicotine

Caffeine and nicotine are not found naturally within the body. Both of these nonregulated drugs have an excitatory effect on membranes of neurons in general and have a stimulatory effect on the cardiac centers specifically, causing an increase in HR. Caffeine works by increasing the rates of depolarization at the SA node, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart.

Although it is the world’s most widely consumed psychoactive drug, caffeine is legal and not regulated. While precise quantities have not been established, “normal” consumption is not considered harmful to most people, although it may cause disruptions to sleep and acts as a diuretic. Its consumption by pregnant people is cautioned against, although no evidence of negative effects has been confirmed. Tolerance and even physical and mental addiction to the drug result in individuals who routinely consume the substance.

Nicotine, too, is a stimulant and produces addiction. While legal and nonregulated, concerns about nicotine’s safety and documented links to respiratory and cardiac disease have resulted in warning labels on cigarette packages.

E. Factors Decreasing Heart Rate

HR can be slowed when a person experiences altered sodium and potassium levels, hypoxia, acidosis, alkalosis, and hypothermia (see Table 1). The relationship between electrolytes and HR is complex, but maintaining electrolyte balance is critical to the normal wave of depolarization. Of the two ions, potassium has the greater clinical significance. Initially, both hyponatremia (low sodium levels) and hypernatremia (high sodium levels) may lead to tachycardia. Severely high hypernatremia may lead to fibrillation, which may cause CO to cease. Severe hyponatremia leads to both bradycardia and other arrhythmias. Hypokalemia (low potassium levels) also leads to arrhythmias, whereas hyperkalemia (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail.

Acidosis is a condition in which excess hydrogen ions are present, and the patient’s blood expresses a low pH value. Alkalosis is a condition in which there are too few hydrogen ions, and the patient’s blood has an elevated pH. Normal blood pH falls in the range of 7.35–7.45, so a number lower than this range represents acidosis and a higher number represents alkalosis. 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. In this case, the patient’s blood is normally diverted to an artificial heart-lung machine to maintain the body’s blood supply and gas exchange until the surgery is complete, and sinus rhythm can be restored. 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.

OpenStax. (2022). Anatomy and Physiology 2e. Rice University. Retrieved June 15, 2023. ISBN-13: 978-1-711494-06-7 (Hardcover) ISBN-13: 978-1-711494-05-0 (Paperback) ISBN-13: 978-1-951693-42-8 (Digital). License: Attribution 4.0 International (CC BY 4.0). Access for free at openstax.org.

Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain. They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus (parasympathetic) nerves that slow cardiac activity.

The wave of depolarization in a normal sinus rhythm shows a stable resting HR. Following parasympathetic stimulation, HR slows. Following sympathetic stimulation, HR increases.

FactorEffect
Cardioaccelerator nervesRelease of norepinephrine by cardioaccelerator nerves
ProprioreceptorsIncreased firing rates of proprioreceptors (e.g. during exercise)
ChemoreceptorsChemoreceptors sensing decreased levels of O2 or increased levels of H+, CO2 and lactic acid
BaroreceptorsDecreased firing rates of baroreceptors (indicating falling blood volume/pressure)
Limbic systemAnticipation of physical exercise or strong emotions by the limbic system
CatecholaminesDecreased epinephrine and norepinephrine release by the adrenal glands
Thyroid hormonesIncreased T3 and T4 in the blood (released by thyroid)
CalciumIncrease in calcium ions in the blood
PotassiumDecrease in potassium ions in the blood
SodiumDecrease in sodium ions in the blood
Body temperatureIncrease in body temperature
Nicotine and caffeinePresence of nicotine, caffeine or other stimulants
FactorEffect
Cardioinhibitor nerves (vagus)Release of acetylcholine by cardioinhibitor nerves
ProprioreceptorsDecreased firing rates of proprioreceptors (e.g. during rest)
ChemoreceptorsChemoreceptors sensing increased levels of O2 or decreased levels of H+, CO2 and lactic acid
BaroreceptorsIncreased firing rates of baroreceptors (indicating rising blood volume/pressure)
Limbic systemAnticipation of relaxation by the limbic system
CatecholaminesDecreased epinephrine and norepinephrine release by the adrenal glands
Thyroid hormonesDecreased T3 and T4 in the blood (released by thyroid)
CalciumDecrease in calcium ions in the blood
PotassiumIncrease in potassium ions in the blood
SodiumIncrease in sodium ions in the blood
Body temperatureDecrease in body temperature
Opiates and tranquilizersPresence of opiates (heroin), tranquilizers or other depressants
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Script:
  1. Many factors affect heart rate and stroke volume, and together, they contribute to cardiac function.
  2. Heart rate is largely determined and regulated by autonomic stimulation and hormones.
  3. 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.
  4. Stroke volume is regulated by autonomic innervation and hormones, but also by filling time and venous return.
  5. Venous return is determined by activity of the skeletal muscles, blood volume, and changes in peripheral circulation.
  6. Venous return determines preload and the atrial reflex.
  7. Filling time directly related to heart rate also determines preload.
  8. Preload then impacts both end diastolic volume and end systolic volume.
  9. Autonomic innervation and hormones largely regulate contractility.
  10. Contractility impacts end diastolic volume as does afterload.
  11. Cardiac output is the product of heart rate multiplied by stroke volume.
  12. Stroke volume is the difference between end diastolic volume and end systolic volume.
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