Introduction to Cardiovascular Physiology
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The physiology of the peripheral circulation is explained in the next three chapters with particular attention paid to endothelial cell function and the control of solute and fluid exchange. The control of vascular smooth muscle and the wider control of blood vessels in response to intrinsic and extrinsic regulation are dealt with in the following three chapters.
The final part of the book includes a chapter looking at specialized circulations followed by chapters on the central control and coordinated cardiovascular responses to normal physiological scenarios such as posture, exercise, and the Valsalva manoeuvre, but also the same responses associated with the conditions of hypertension, hypovolaemic shock, and cardiac failure. Within each chapter, the author makes a wide use of clear diagrams to complement and help explain the text.
The text of the chapters themselves is regularly broken down into smaller sections focusing on particular points. Throughout the text, key words are highlighted with the use of a bold font. Although some readers may dislike this layout, I feel it allows you to focus on the points being explained. The appearance of the text together with specificity of individual chapters means it is quite easy to pick this book up and read through a single chapter relatively quickly.
At the end of each chapter, the author has included a useful summary of points covered and a reference list for further reading. An added benefit of purchasing this book is that it allows access to an online resource provided by the publisher. This contains a series of self-assessment single best answer type questions, a number of powerpoint presentations, and electronic access to references used in each chapter. The reader will also find electronic copies of all diagrams used within the book.
These are printable and downloadable and I expect will form a very useful teaching tool.
Mainardi, L. Human Physiology, Biochemistry and Basic Medicine. Seller Inventory BBI Close mobile search navigation Article Navigation. Hinrich Staecker. Umetani, K. Jr, Mohanty, P.
Is this textbook relevant or of use to anaesthetists? Initially, a reader might be a bit intimidated by a book of more than pages, which focuses solely on just cardiovascular physiology. Shop Textbooks.
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Temporarily Out of Stock Online Please check back later for updated availability. Overview A good understanding of cardiovascular physiology is fundamental to understanding cardiovascular disease, exercise performance, and many other aspects of human physiology. Average Review. Bradycardia may be caused by either inherent factors or causes external to the heart. While the condition may be inherited, typically it is acquired in older individuals. Inherent causes include abnormalities in either the SA or AV node.
If the condition is serious, a pacemaker may be required. Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves. External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest.
Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen. Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the autonomic nervous system.
In some cases, tachycardia may involve only the atria. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting syncope. While tachycardia is defined as a HR above bpm, there is considerable variation among people. Further, the normal resting HRs of children are often above bpm, but this is not considered to be tachycardia Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation.
Elevated rates in an exercising or resting patient are normal and expected. Resting rate should always be taken after recovery from exercise. Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery. 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 bpm, CO will rise.
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As HR increases from to bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. 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 and 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 2. 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.
Heart: Broken Heart Syndrome
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 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.
Introduction to Complex Cardiovascular Physiology
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 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.
Summary. A sound knowledge of cardiovascular physiology is fundamental to understanding cardiovascular disease, exercise performance and may other. Publisher Summary. This chapter provides an overview of the cardiovascular system. The rate at which diffusional transport occurs is critically important because.
In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately bpm. Any increases beyond this rate would require sympathetic stimulation. Figure 3 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.
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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. Extreme stress from such life events as the death of a loved one, an emotional break up, loss of income, or foreclosure of a home may lead to a condition commonly referred to as broken heart syndrome.
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