September 26, Share on Facebook Share on Twitter. Students can also link to the author's regularly updated Web site for additional clinical information. Suitable for USMLE and exam review, this title helps you gain a fundamental knowledge of the basic operating principles of the intact cardiovascular system and how those principles apply to clinical medicine.
Current Concepts in Cardiovascular Physiology examines seven different areas related to the field of cardiac physiology. In addition to the biochemistry and receptor pharmacology of the heart, this book explores coronary physiology, cardiovascular function, and neural and reflex control of the circulation.
The electrophysiology and biophysics of cardiac excitation are also considered, along with humoral control of the circulation. This monograph consists of seven chapters and opens with an overview of the biochemistry of the heart, with emphasis on cardiac energy metabolism and the ways in which metabolism and the biochemical pathways are controlled.
The mechanisms whereby physiological events influence biochemical activities and vice versa are also discussed. The following chapters look at the chemistry and physiology of myocardial receptors; the complex interplay between the nervous and cardiovascular systems; and the chemical and hormonal factors that regulate, modify, and modulate the cardiovascular system.
The influence of humoral, neural, intrinsic, vascular, and myocardial factors on coronary blood flow is also examined, along with muscle mechanics; the biochemical basis of contraction; cardiac function; and the factors determining the heart's electrophysiologic behavior.
This text is directed primarily at clinical cardiologists, cardiovascular surgeons, and trainees in their disciplines, as well as internists, medical students, and house officers. This title is directed primarily towards health care professionals outside of the United States. Written by an eminent cardiovascular physiologist with a strong track record in dealing with issues related to exercise and environmental physiology, this text covers cardiovascular function from the exercise and human physiologist's viewpoint.
It provides a solid foundation of knowledge of how the cardiovascular system responds and adapts to the challenges of exercise and environmental change, and analyses the practicalities of measuring cardiovascular parameters in normal human subjects. Case studies in exercise physiology throughout text. Open-ended questions at end of each chapter encourage students to explore common situations facing exercise and human physiologists. Bibliography at end of each chapter directs students to further reading resources.
Summaries at start of each chapter and multiple choice questions with explanatory answers at end of book aid revision and help students test their knowledge. Skip to content. Cardiovascular Physiology. Cardiovascular Physiology Concepts. Cardiovascular Physiology Concepts Book Review:. Author : Achilles J. Buja teaches medical students, medical residents, clinical fellows, graduate students and research post-doctoral fellows.
He also conducts a clinical practice in cardiovascular pathology providing staffing of autopsy cases and surgical pathology consultation of cardiac and vascular cases and interpretation of myocardial biopsies from referrals. He directs a cardiovascular pathology fellowship approved by the Texas Medical Board.
Since the establishment of an Advanced Heart Failure Center on campus, he has served as the cardiovascular pathologist for the Center and has provided staffing for over heart transplants, numerous LVADs, and post-transplant myocardial biopsies for evaluation and grading of antibody-mediated and acute cellular rejection.
Buja serves as a consultant in cardiovascular pathology for the Harris County Institute of Forensic Sciences. He serves as the Director of the DPALM Autopsy Service at the affiliated teaching hospitals and has been an advocate of the importance of the autopsy as a tool in medical research and quality control in healthcare. The end product of metabolism of glycogen, glucose, fatty acids, triglycerides, pyruvate, and lactate is acetyl CoA, which enters the citric acid Krebs cycle in the mitochondria, where, by a process of oxidative phosphorylation, the molecules are degraded to carbon dioxide and water and the energy is converted to ATP.
The student is encouraged to consult a biochemistry textbook for further details of these important metabolic pathways. The heavy nearly total reliance of the heart on the aerobic pathways for ATP production is evident by I the high number of mitochondria and 2 the presence of high concentrations of the oxygen-binding protein myoglobin within the cardiac muscle cells. Myoglobin can release its oxygen to the mitochondrial cytochrome oxidase system when intracellular oxygen levels are lowered.
It is important to understand what factors determine the energy costs and, therefore, the myocardial oxygen consumption rate because reduction of the oxygen demand may be of significant clinical benefit to the patient.
Because the heart derives its energy almost entirely from aerobic metabolism, myocardial oxygen consumption is directly related to myocardial energy use ie, ATP splitting. Because basal metabolism represents the energy consumed in cellular processes other than contraction eg, energy-dependent ion pumping , little can be done to reduce it. P rimarily, this ref lects ATP splitting associated with cross-bridge cycling during the isovolumetric contraction and ejection phases of the cardiac cycle.
Cardiac afterload then is a major determinant of myocardial oxygen consumption. Reductions in cardiac afterload can produce clinically significant reductions in myocardial energy requirements and therefore myocardial oxygen consumption.
Energy utilization during isovolumetric contraction is actually more directly related to isometric wall tension development than to intraventricular pressure development. The external physical work done by the left ventricle in 1 beat, called stroke work, is equal to the area enclosed by the left ventricular pressure-volume loop see Figure Stroke work is increased either by an increase in stroke volume increased "volume" work or by an increase in afterload increased "pressure" work.
Thus, reductions in afterload are especially helpful in reducing the myocardial oxygen requirements for doing external work.
Changes in myocardial contractility can have important consequences on the oxygen requirement for basal metabolism, isovolumic wall tension generation, and external work. Heart muscle cells use more energy in rapidly developing a given tension and shortening by a given amount than in doing the same thing more slowly. The net result of these influences is often referred to as the "energy wasting" effect of increased contractility.
The heart rate is one of the most important determinants of myocardial oxygen consumption because the energy cost per minute must equal the energy cost per beat times the number of beats per minute. In general, it has been found that it is more efficient ie, less oxygen is required to achieve a given cardiac output with the low heart rate and high stroke volume than with the high heart rate and low stroke volume.
This again appears to be related to the relatively high energy cost of the pressure development phase of the cardiac cycle. The job of the heart is to establish the pressure that drives blood passively through the pulmonic and systemic circulations.
This is a remarkable, highly efficient, adaptable, and long-lasting pump that we, despite our best efforts, are unable to duplicate with any significant degree of success. When it breaks down, we suffer rather immediate adverse consequences. Much of our current medical interventions are aimed at the coronary vasculature. Description of coronary flow is presented in more detail in Chapter 8. In this book, we have ignored the extracellular structures of the heart, that is, the fibrous valves, the connective tissue frame cardiac skeleton that functions to electrically isolate the atria from the ventricles, and the extracellular matrix that forms a dynamic scaffolding surrounding the contractile cells.
These structures are made primarily of collagen from the fibroblasts and not only maintain the structural integrity of the heart but appear to participate importantly in dynamic adaptations to changing conditions.
There is current interest in the influence of the extracellular matrix components on cardiac behavior. KEY CONCEPTS Effective cardiac pumping of blood requires coordinated filling of the chambers, excitation and contraction of the cardiac muscle cells, pressure generation within the chambers, opening and closing of cardiac valves, and one-way movement of blood through the chambers into the aorta or pulmonary artery. Stroke volume can be altered by changes in ventricular preload filling , ventricular.
Ventricular Dejection fraction" describes the fraction of end-diastolic volume of. Because pulmonary artery pressure is so much lower than aortic pressure, the right ventricle has a larger stroke volume than the left ventricle. Which of the following interventions will increase cardiac stroke volume?
In which direction will cardiac output change if central venous pressure is lowered while cardiac sympathetic tone is increased? Four of these conditions exist during the same phase of the cardiac cycle and one does not. Which one is the odd one? The mitral valve is open. The "v" wave of thejugular venous pulse hasjust occurred.
Ventricular volume is increasing. Aortic pressure is falling. With all other factors equal, myocardial oxygen demands will be increased to the greatest extent by which of the following? Sympathetic neural activation of the heart will decrease which of the following? PR interval on the ECG c. There are a variety of methods available to assess cardiac function. This chapter provides a brief overview of some of these commonly used clinical tools.
Advances i? Visual or computer-aided analysis of such images provides information useful in clinically evaluating cardiac function. These techniques are especially suited for detecting abnormal operation of cardiac valves or contractile.
They can also provide estimates of heart chamber volumes at different times in the cardiac cycle that are used to assess cardiac function. This noninvasive technique is based on the fact that sound waves reflect back toward the source when encountering abrupt changes in the density of the medium through which they travel. The longer the time between the transmission of the wave and the arrival of the reflection, the deeper the structure is in the thorax. Such information can be reconstructed by computer in various ways to produce a continuous image of the heart and its chambers throughout the cardiac cycle.
Doppler echocardiography can provide additional information about blood flow velocity and direction across the cardiac valves. It is particularly useful in detecting valve stenosis or insufficiency. Other imaging techniques are available for assessing cardiac function. A gamma camera is used to obtain images collected at ie, gated to different times in the cardiac cycle.
Decreases in contractility as may be caused by heart disease are associated with a downward shift of the line, discussed further in Chapter Cl I E. The effect of increased contractility on the left ventricular end-systolic pressure-volume relationship. Thus, it is possible to get a reasonable clinical estimate of the slope of the end-systolic pressure-volume relationship read "myocardial contractility" from a single measurement of end-systolic pressure and volume.
This avoids the need to do multiple tests with vasodilator or vasoconstrictor infusions. Pick principle: The most accurate but unfortunately somewhat invasive way of measuring how much blood is actually pumped by the heart per minute is by the use of the Fick principle described in Chapter 1. A common method of determining cardiac output is to use the Fick principle to calculate the collective flow through all systemic organs from I the whole body oxygen consumption rate Xtc by monitoring the oxygen uptake from inspired air , 2 the oxygen concentration in arterial blood [X] , obtained from any convenient arterial puncture , and 3 the concentration of oxygen in mixed venous blood [X]j which is the most difficult to obtain.
The calculation of cardiac output from the Fick principle is best illustrated by an example. Suppose that a patient is consuming mL of 02 per minute when his or her systemic arterial blood contains mL of 02 per liter and the right ventricular blood contains mL of 02 per liter.
In order for mL of 02 to be consumed per minute, 5 L of blood must pass through the systemic circulation each minute:. It is possible to estimate the cardiac output from the quantity of indicator injected and the time record of indicator concentration in the blood that leaves the left side of the heart.
Echocardiography is also used to estimate cardiac output. Information about cardiac output can be obtained from the product of these estimates of stroke volume and heart rate. A variety of other methods for estimating cardiac output have been used and may provide useful assessments under various conditions. Therefore, it is common to express the cardiac output per square meter of surface area. It does not provide specific information about mechanical activity. As briefly described in Chapter 2, the electrocardiogram is the result of currents propagated through the extracellular fluid that are generated by the spread of the wave of excitation throughout the heart.
Electrodes placed on the surface of the body record the small potential differences between various recording sites that vary over the time course of the cardiac cycle.
A typical electrocardiographic record is indicated in Figure The period from the initiation of the P wave to the beginning of QRS complex is designated as the PR interval and indicates the time it takes for an action potential to spread through the atria and the atrioventricular AV node. During the latter portion of the PR interval PR segment , no voltages are detected on the body. PR interval QT interval. Typical electrocardiogram of a single cardiac cycle. This is because atrial muscle cells are depolarized in the plateau phase of their action potentials , ventricular cells are still resting, and the electrical field set up by the action potential progressing through the small AV node is not intense enough to be detected.
The duration of the normal PR interval ranges from to ms. Shortly after the cardiac impulse breaks out of the AV node and into the rapidly conducting Purkinje system, all the ventricular muscle cells depolarize within a very short period and cause the QRS complex. The normal QRS complex lasts between 60 and ms. Myocardial injury or inadequate blood flow, however, can produce elevations or depressions in the ST segment.
When ventricular cells begin to repolarize, a voltage difference once again appears on the body surface and is measured as the T wave of the electrocardiogram. The T wave is broader and not as large as the R wave because ventricular repolarization is less synchronous than depolarization.
At the conclusion of the T wave, all the cells in the heart are in the resting state. The QT interval roughly approximates the duration of ventricular myocyte action potential and thus the period of ventricular systole.
No body surface potential is measured until the next impulse is generated by the sinoatrial SA node. It should be recognized that the operation of the specialized conduction system is a primary factor in determining the normal electrocardiographic pattern. For example, the AV nodal transmission time determines the PR interval. Also, the effectiveness of the Purkinje system in synchronizing ventricular depolarization is reflected in the large magnitude and short duration of the QRS complex.
It should also be noted that nearly every heart muscle cell is inherently capable of rhythmicity and that all cardiac cells are electrically interconnected through gap junctions. Thus, a functional heart rhythm can, and often does, occur without the involvement of part or all of the specialized conduction system. Such a situation is, however, abnormal, and the existence of abnormal conduction pathways would produce an abnormal electrocardiogram.
Recording electrodes are placed on both arms and the left leg-usually at the wrists and the ankle. The appendages are assumed to act merely as extensions of the recording system, and voltage measurements are assumed to be made between points that form an equilateral triangle over the thorax, as shown in Figure Any single electrocardiographic trace is a recording of the voltage difference measured between any 2 vertices of Einthoven's triangle.
An example of the lead II electrocardiogram measured between the right arm and the left leg has already been shown in Figure Similarly, lead I and lead III electrocardiograms represent voltage measurements taken along the other two sides ofEinthoven's triangle, as indicated in Figure Conversely, a downward deflection in a lead II record indicates that a polarity exists between the electrodes at that instant, with the left leg electrode being negative.
As shown in the next chapter, many cardiac electrical abnormalities can be detected in recordings from a single electrocardiographic lead. However, certain clinically useful information can be derived only by combining the information obtained from two electrocardiographic leads.
To understand these more complex electrocardiographic analyses, a close examination of how voltages appear on the body surface as a result of the cardiac electrical activity must be done. Einthoven's conceptualization of how cardiac electrical activity causes potential differences on the surface of the body is illustrated in Figure The cardiac impulse, after having arisen in the SA node, is spreading as a wavefront of depolarization through the atrial tissue. At each point along this wavefront of electrical activity, a small charge separation exists in the extracellular fluid between polarized membranes positive outside and depolarized membranes negative outside.
Thus, the wavefront may be thought of as a series of individual electrical dipoles regions of charge separation. Each individual dipole is oriented in the direction of local wavefront movement. The salty extracellular fluid acts as an excellent conductor, allowing these instantaneous net dipoles, generated on the surface of the heart muscle to be recorded by electrodes on the surface of the body. The net dipole that exists at any instant during depolarization is oriented ie, points in the general direction of wavefront movement at that instant.
Net cardiac dipole during atrial depolarization and its components on the limb leads. The net dipole in the example in Figure causes the lower-left portion of the body to be generally positive with respect to the upper-right portion. As shown in the right half of Figure , this can be deduced from Einthoven's triangle by observing that the net dipole has some component that points in the positive direction of leads I, II, and III.
As illustrated in Figure , the component that a cardiac dipole has on a given electrocardiogram lead is found by drawing perpendicular lines from the appropriate side of Einthoven's triangle to the tip and tail of the dipole. Note that the dipole in this example is most parallel to lead II and therefore has a large component in the lead II direction. The limb lead configuration may be thought of as a way to view the heart's electrical activity from three different perspectives or axes. The instantaneous voltage measured on the axis of lead I, for example, indicates how the dipole being generated by the heart's electrical activity at that instant appears when viewed from directly above.
Thus, it is necessary to have views from 2 directions to establish the magnitude and orientation of the heart's dipole. It is important to emphasize that the example in Figure pertains only to one instant during atrial depolarization.
The net cardiac dipole continually changes in magnitude and orientation during the course of atrial depolarization. The nature of these changes will determine the shape of the P wave on each of the electrocardiogram leads. The P wave terminates when the wave of depolarization, as illustrated in Figure , reaches the nonmuscular border between the atria and the ventricles and the number of individual dipoles becomes very small.
At this time, the cardiac impulse is still being slowly transmitted toward the ventricles through the AV node. However, the electrical activity in the AV node involves so few cells that it generates no detectable net cardiac dipole. Thus, no voltages are measured on the surface of the body for a brief period following the P wave.
A net cardiac dipole reappears only when the depolarization completes its passage through the AV node, enters the Purkinje system, and begins its rapid passage over the ventricular muscle cells. Ventricular Depolarization and the QRS Complex It is the rapid and large changes in the magnitude and direction of the net cardiac dipole that occur during ventricular depolarization that cause the QRS complex of the electrocardiogram.
The normal process is illustrated in Figure Analysis of the. Ventricular depolarization and the generation of the QRS complex. The upper-right panel shows the actual deflections on each of the electrocardiographic limb leads that will be produced by this dipole. Note that it is possible for a given cardiac dipole to produce opposite deflections on different leads. This phase generates the large net cardiac dipole, which is responsible for the R wave of the electrocardiogram.
In Figure , this net cardiac dipole is nearly parallel to lead II. As indicated, such a dipole produces large positive R waves on all three limb leads. The third row in Figure shows the situation near the end of the spread of depolarization through the ventricles and indicates how the small net cardiac dipole present at this time produces the S wave. Note that an S wave does not necessarily appear on all electrocardiogram leads as in lead I of this example. There are no waves of electrical activity moving through the heart tissue.
Consequently, no net cardiac dipole exists at this time and no voltage differences exist between points on the body surface. All electrocardiographic traces will be flat at the isoelectric zero voltage level. This indicates that the net cardiac dipole generated during ventricular repolarization is oriented in the same general direction as that existing during ventricular depolarization.
This may be somewhat surprising. However, recall from Figure that the last ventricular cells to depolarize are thefirst to repolarize. The reasons for this are not well understood, but the result is that the wavefront of electrical activity during ventricular repolarization tends to retrace, in reverse direction, the course followed during ventricular depolarization.
The T wave is broader and smaller than the R wave because the repolarization of ventricular muscle cells is less well synchronized than is their depolarization. The orientation of the cardiac dipole during the most intense phase of ventricular depolarization ie, at the instant the R wave reaches its peak is called the mean electrical axis of the heart.
Note that the downward direction corresponds to plus 90 degrees in this polar coordinate system. As indicated, a mean electrical axis that lies anywhere in the patient's lower left-hand quadrant is considered normal. A left-axis deviation exists when the mean electrical axis falls in the patient's upper left-hand quadrant and may indicate a physical displacement of the heart to the left, left ventricular hypertrophy, or loss of electrical activity in the right ventricle.
A right-axis deviation exists when the mean electrical axis falls in the patient's lower right-hand quadrant and may indicate a physical displacement of the heart to the right, right ventricular hypertrophy, or loss of electrical activity in the left ventricle. The process involves determining what single net dipole orientation will produce the R-wave amplitudes recorded on any two leads. As should be obvious, in this case, the amplitude of the R wave on lead I will be zero.
In Figure , for example, the largest R wave occurs on lead II. Another analysis technique called vectorcardiography is based on continuously following the magnitude and orientation of the heart's dipole throughout the. A typical vectorcardiogram is illustrated in Figure and is a graphical record of the dipole amplitude in the x and y directions throughout a single cardiac cycle.
The first small loop is caused by atrial depolarization, the second large loop is caused by ventricular depolarization, and the final intermediate-sized loop is caused by ventricular repolarization. Analogous "mean axes" can similarly be defined for the P wave and T wave but are not commonly used. The other 9 leads are unipolar leads.
Three of these leads are generated by using the limb electrodes. Two of the electrodes are electrically connected to form an indifferent electrode, whereas the third limb electrode is made the positive pole of the pair.
Detail explanation of cardiovascular physiology to diagnosis and treatment. There is concise summarizes key concepts at the end of each chapter. Comprehensive highlights must-know information with chapter objectives.
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