Page Anticoagulation strategies Page ECMO transport Page Ethical considerations Postoperative Care of the Cardiac Surgical Patient Page The transport process Page Transition to ICU monitors Page The actual handoff Page Pulmonary changes after sternotomy and thoracotomy Page Choosing modes of ventilation Page Liberation from mechanical ventilation Page Methods of fast tracking Page Goals of enhanced recovery after cardiac surgery Page Monitoring for ischemia Page Ventricular dysfunction after cardiac surgery Page Fluid management Page Managing hypotension Page Dysrhythmia management Page Nerve blocks Page Sedation Page Electrolyte abnormalities Page Shivering Page Glucose management Page Bleeding Page Cardiac tamponade Page Acute graft closure Page Postoperative neurologic dysfunction Page Patients with mechanical assist devices Page Ventricular assist device VAD Page The preoperative discussion Page The role of family support Protection of the Brain During Cardiopulmonary Bypass Page Stroke incidence Page Early versus delayed stroke Page Cognitive dysfunction Page Comparison groups Page Delirium Page Cerebral autoregulation CA Page pH management Page Embolization Page Hypoperfusion Page Brain temperature Page Electroencephalogram EEG Page Cerebral perfusion pressure CPP Page Prevention of central nervous system CNS injury Page Open-chamber de-airing techniques Page Euglycemia Page Pharmacologic cerebral protection Page Metabolic suppression Page Clinical indications Page Brain protection Page Morbidity Pain Management for Cardiothoracic Procedures Page Incidence and severity of pain after cardiothoracic procedures Page Transmission pathways for nociception Page Analgesia considerations: the procedure, patient, and process Page Outcome benefits of good analgesia for cardiothoracic procedures Page Opioid analgesics Page Acetaminophen paracetamol Page Local anesthetics Page Gabapentinoids Page Intercostal Page Fascial plane blocks Page Intrathecal IT Page Epidural Page Off-pump sternotomy cardiac procedures Page Nausea and vomiting Page Respiratory depression Page Infectious complications Page Intrathecal IT morphine Page Index This book is protected by copyright.
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Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources.
While preparing this manual, he recognized the wider need for a point-of-care reference book on cardiac anesthesia. He then sought to address this deficiency by compressing a readable, comprehensive cardiac anesthesia textbook into a pocket-sized paperback package. Its mission would be to provide clinical recommendations supported by their briefly-explained underlying scientific principles. Practical clinical relevance and conciseness were deemed more important than lengthy narratives and prodigious reference lists.
Hensley recruited his Hershey friend and colleague, Donald E. Martin, MD, to co-edit this book. Together they envisioned a multiauthor text representing multiple teaching hospitals, so they recruited chapter authors who were recognized for clinical expertise and experience.
To achieve thoroughness without sacrificing readability, Rick and Don thought that the chapters should be formatted as outlines. As editors, they delicately pursued practical clinical advice while avoiding parochial institutional practices.
Their vision flew in the face of the prevailing approach to both medical textbooks and handbooks. At the time, comprehensive medical textbooks predominantly were lengthy tomes with thousands of references. Hardly anything existed between those extremes.
The book was warmly received by busy residents and fellows. Residency and fellowship program directors embraced it for its unique blend of quality, thoroughness, and conciseness. Chronology of Frederick A. Cleveland, Jr. Cooper, Jr. Luck, Jr. McLoughlin, Jr. The subspecialty of cardiothoracic anesthesiology continues to evolve, just as this book aspires to evolve with it. As it was for the first edition in , our mission is to provide an easily accessible, practical reference to help trainees and practitioners prepare for and manage anesthetics within the subspecialty.
Each new editor brings a fresh and multi-institutional perspective that includes expertise in cardiothoracic anesthesia and critical care as well as clinical experience in both North America and Europe.
Bartels also offers expertise in perioperative acute and chronic pain management. This edition also adds 23 links to video clips spread across Chapters 5, 11, 12, and In addition to the Key Points at the beginning of each chapter locations marked in text margins also , all chapters now include several Clinical Pearls, which are short, key clinical concepts located in the text section where their subject matter is presented. Highlighting of key references constitutes another new feature.
Although we tried to keep overlap between chapters to a minimum, we allowed it when we believed that differences in content or perspective merited retention.
The sections have been subtly reorganized to flow from basic science on to general tenets of intraoperative management, then to specific cardiothoracic disorders, and to conclude with sections on circulatory support and perioperative management. Some previous chapters have been reconfigured or merged, such as Induction of Anesthesia and Precardiopulmonary Bypass Management Chapter 6 and Anesthetic Management of Cardiac and Pulmonary Transplantation Chapter A chapter on blood management supersedes one on blood transfusion.
The growth of minimally invasive valve procedures inspired the creation of a separate chapter for aortic valve procedures as well as one for those involving the mitral and tricuspid valves, each with the addition of video clips emphasizing echocardiography. Rapid development of extracorporeal membrane oxygenation in adults now merits a full chapter.
Robotic surgical techniques for cardiac and thoracic surgery earn expanded coverage in Chapter We decided to concede the huge topic of congenital heart disease in children to other textbooks, while retaining and updating the one on adult congenital heart disease.
Glenn P. Gravlee, MD Andrew D. The editors thank the 69 authors representing 37 institutions for their timely and tireless efforts. On the publishing side, we thank Wolters Kluwer for their continued support of this book. In particular, Keith Donellan gets warm thanks and appreciation for his dedication, experience, and wisdom. Special thanks go to Louise Bierig, whose expertise, persistence, and detail orientation during developmental editing proved indispensable.
Gayeski 2. Desai, Alann Solina, Donald E. Martin, and Kinjal M. Patel 4. Gerhardt and Andrew N. Springer 5. Transesophageal Echocardiography Jack S. Shanewise 6. Mehta, Michael G. Licina, and Glenn P. Gravlee 7. Management of Cardiopulmonary Bypass Neville M. Gibbs, Shannon J.
Matzelle, and David R. Larach 8. Morris, Chandrika R. Garner, and Roger L. Royster 9. Blood Management Nadia B. Hensley, Megan P. Kostibas, Steven M. Frank, and Colleen G. Green, Gary Okum, and Jay C. Horrow Tuck and Matthew M. Townsley Mahmood Mehta, Peter Slinger, James G.
Ramsay, Javier H. Campos, and Michael G. Licina Fox and John R. Sullivan Davies, S. Adil Husain, and Nathaen S. Weitzel Anton, Anne L. Rother, Charles D. Collard, and Erin A. Samii and Jerry C. Hull and Matthew M. Hessel, II Nini Malayaman, Jay C. Horrow, Glenn P. Gravlee, and Linda Shore-Lesserson Hoffman, Jay D. Pal, and Joseph C. Sullivan and Michael H. Wall Murkin Bottiger, Rebecca Y.
Klinger, Thomas M. Gayeski I. Introduction II. Embryologic development of the heart III. Electrical conduction IV. Cardiac myocyte A. Sarcomere V. Organization of myocytes VI. Length—tension relationship VII. A heart chamber and external work A. The chamber wall B.
Atria C. Ventricle D. Preload and compliance E. Ventricular work F. Starling curve G. Myocardial oxygen consumption VIII. Control systems IX. The cardiovascular control system X. Stretch receptors: Pressure sensors XI. Atrial baroreceptors XII. Arterial baroreceptors XIII. Effectors and physiologic reserves for the healthy individual XIV. The cardiovascular system integration XV. Effect of anesthesia providers and our pharmacology on the cardiovascular system A.
The surgical patient B. The anesthetic choice C. The heart has a fibrous skeleton that provides an insertion site at each valvular ring. The fundamental unit of tension development is the sarcomere.
The endocardium receives blood flow only during systole while the epicardium receives blood flow throughout the cardiac cycle. The endocardium is more susceptible to infarction. Oxygen or ATP consumption occurs during release of actin— myosin bonds during relaxation of this bond.
The main determinants of myocardial oxygen consumption are heart rate HR , contractility, and wall tension. The external stroke volume SV work the ventricle does is to raise the pressure of a SV from ventricular end-diastolic pressure VEDP, right or left to mean arterial pressure pulmonary or systemic, respectively. The cardiovascular system regulates blood pressure BP and exemplifies a negative feedback loop control system. Sensors throughout the cardiovascular system detect pressure through stretch.
Hence, compliance changes impact pressure sensors. Physiologic reserves are expansion factors allowing the cardiovascular system to maintain BP.
Venous capacitance reserve is approximately 1, mL in a 70kg adult. Introduction As a physiologic primer for cardiac anesthesiology, this chapter requires compromise and choices! The studies of cardiac anatomy, physiology, pathology, and genomics are decades to centuries old, continue to evolve, and have a vast literature. Our focus is on presenting physiologic principles important to adult clinical management in the operating room OR.
The first compromise is that I will barely touch embryology and I chose not to discuss pediatric cardiac physiology. To complement our view, a detailed description and discussion of adult cardiac physiology can be found in Ref. A thorough understanding of the physiologic concepts contained herein will facilitate the anesthetic care of both healthy patients and those with cardiovascular disease. Embryologic development of the heart A.
The cardiovascular system begins to develop during week 3 of gestation as the primitive vascular system is formed from mesodermally derived endothelial tubes. At week 4, bilateral cardiogenic cords from paired endocardial heart tubes fuse into a single heart tube primitive heart.
The primitive heart evolves into four chambers: Bulbus cordis, ventricle, primordial atrium, and sinus venosus, eventually forming a bulboventricular loop with initial contraction commencing at 21 to 22 days. These contractions result in unidirectional blood flow in week 4. From weeks 4 to 7, heart development enters a critical period, as it divides into the fetal circulation and the four chambers of the adult heart. A fibrous skeleton composed of fibrin and elastin forms the framework of four rings encircling the four heart valves as well as intermyocyte connections.
The fibrous skeleton 1. Resists overdistention of the annuli of the valves resisting incompetence 3. Provides a fixed insertion point for the muscular bundles of the ventricles 4. Minimizes intermyocyte sliding during ventricular filling and contraction III.
Electrical conduction A. This speed difference results in coordinated chamber contraction. Purkinje fibers exist in the atrium and ventricles in the subendocardium. Hence, they can be accessed from within the respective chambers.
The fibrous skeleton slows the direct spread of electrical conduction between myocytes as well as between atrium and ventricles. Coordinated chamber contraction depends on Purkinje signal conduction, not on intermyocyte conduction.
This sequence consists of a coordinated contraction in the atrium followed by a delay as the Purkinje signal passes through AV node, which is in turn followed by coordinated contraction of ventricles.
Action potential 1. A membrane potential is the difference in voltage between the inside of the cell and the outside. In a cell this membrane potential is a consequence of the ions and proteins inside and outside the cell.
At rest, potassium ions can cross the membrane readily while sodium and chloride ions have a greater difficulty in doing so. They open or close in response to a stimulus, most frequently a chemical stimulus. Membrane differences in ion channel concentrations and characteristics are cell-type specific. At rest, the negative ions within the cell predominate, resulting in a negative transmembrane voltage. The resting voltage is referred to as the resting membrane potential. A- represents negatively charged proteins within the cell.
Under normal conditions at rest, membrane potentials are negative, meaning that the voltage is more negative within the cell than outside of it. Stimulation of a cell results in a change in membrane potential characteristic for that cell type because of a choreographed sequence of ion channels opening and closing. The plot of this sequence is referred to as an action potential. Excitation—contraction coupling in the heart 1.
The intricacies of ion channel opening due to a Purkinje action potential are beyond the scope of this chapter. However, these intricacies are important for anesthesiologists, because clinicians prescribe and administer drugs that directly affect their characteristics.
This graded response is very different than the all-or-none response of skeletal muscle. The SRL and C overlie the myofilaments; they are shown separately for illustrative purposes. From Honig C. Modern Cardiovascular Physiology. This change allows actin and myosin to interact, resulting in shortening of a sarcomere Fig. As compared to extracellular pH, intracellular pH is greatly buffered because of intracellular proteins. Intracellular pH is normally less than extracellular pH.
When either intracellular or extracellular pH changes, transmembrane reequilibration occurs. Because of the greater intracellular buffering capacity, the rate of intracellular pH change is delayed relative to extracellular pH changes.
Sarcomere 1. Actin molecules link to form a chain and two chains intertwine to form a helix. Within each groove of this helix, tropomyosin sits with troponin bound to it intermittently along its length.
This complex is known as a thin filament. In the absence of calcium, the actin sites of the thin filament are not available for binding to myosin. About midway along the thin filament, the Z disc anchors the thin filaments in place in a regular pattern as schematized below. The Z disc is a strong meshwork of filaments that forms a band to anchor the interdigitated thin filaments.
Myosin molecules aggregate spontaneously, thereby forming the thick filaments. These filaments are approximately 1.
These thick filaments are held in place by M filaments and are interdigitated among the thin filaments. During exposure of unbound actin to myosin, they bind together to shorten a sarcomere. After this binding, uncoupling occurs because of the ATPase bound to myosin. This energy-dependent step, requiring oxygen consumption, occurs multiple times within each sarcomere during a cardiac cycle. As long as actin and myosin continue to bind and unbind, the actin—myosin complex continues to shorten the sarcomere as the ventricular chamber contracts in systole.
Intracellular calcium concentration establishes how many actin—myosin sites interact at any instant. The sarcomere length Z-disc separation length establishes the maximum number of actin and myosin heads that could potentially interact at any instant. Increasing the number of heads that do interact results in an increase in contractility see below. Organization of myocytes A. Hence, each myocyte only has about 6 sarcomeres in series from end to end. Each cardiac capillary is approximately 1 mm in length, hence it serves about 80 cardiac myocytes along its length.
As mentioned under embryology, collagen fibers link cardiac myocytes together. In a given layer, myocytes are approximately in parallel. These collagen fiber links connect adjacent, parallel myocytes and form a skeleton. This collagen structure also limits the cardiac myocyte from being overstretched, thereby minimizing the risk of destroying a cell or reducing actin—myosin exposure through overstretching [Ref.
To add complexity, longitudinal alignment of the cardiac myocytes differs in overlapping layers from epicardium to endocardium. Hence, shortening in each layer results in distortion between the layers. Consequently, the endocardium is more vulnerable to ischemia than the epicardium. Blood flow to the endocardium occurs primarily during systole while that to the epicardium occurs during the entire cardiac cycle.
Length—tension relationship A. Consider this thought experiment. As the cardiac myocyte length changes, the length of each sarcomere changes proportionately. This single myocyte is suspended so that a strain gauge measures the tension that the myocyte generates at rest and during contraction. Bottom graph represents percent of maximum tension development versus sarcomere length for strips of cardiac muscle. Note that the fibrous cardiac skeleton inhibits sarcomere stretch from approaching a sarcomere length of 2.
Modified from Honig C. The idealized myocyte is stretched between two fixed points. The tension caused by the force of stretching the muscle at rest and created by the muscle during contraction is measured. The muscle is stretched at rest over a range of Consequently, the sarcomere lengths vary between 1. Plotting resting tension as a function of length results in a resting length— passive tension plot.
Compliance 1. In our idealized myocyte model, a measured amount of tension resulted when the sarcomere was stretched between 1. In plotting this passive tension resulting from passive stretch of the sarcomeres, note that there is very little passive tension required to stretch the sarcomeres until the compliance of the cell membrane started to play a role.
As the sarcomeres become stretched beyond 2. The fibrous skeleton resistance to stretch results in a rapid change in tension with very little change in length very low compliance. The slope of the line of this resting relationship between length and tension is the equivalent of ventricular compliance as will be discussed below.
Contractility 1. In considering the family of curves in the context of ventricular contractility, the contractility is higher when for any given length the developed tension is greater. In vivo, determining contractility of the ventricle is complicated by the interactions of preload and afterload on any measurements.
The SR response is graded. Oxygen consumption 1. As described above, each interaction of actin and myosin results in a submicron shortening of the sarcomere. Each submicron interaction requires ATP for release of the actin—myosin head. It is relaxation of the actin—myosin interaction that requires energy and consumes oxygen.
Remember that the more actin—myosin cycles in a unit of time, the greater the oxygen consumption! The three main determinants of myocardial oxygen consumption are: a. HR: more beats at the same number of actin—myosin interactions b. Contractility: more interactions per beat c. The chamber wall 1. To form a ventricular chamber, individual myocytes are joined together via collagen fibrin strands.
This joining of myocytes, along a general orientation but not end to end, results in a sheet of muscle with myocytes oriented along a similar axis. Several such layers form the ventricular wall. These layers insert on the valvular annuli.
Because of the rapid electrical distribution of the signal through the Purkinje system, the layers contract synchronously resulting in shortening of the muscle layers and a reduction in the volume of the chamber itself. Atria 1. In addition to the volume itself, the rate of ventricular volume addition resulting from atrial contraction may play a role in ventricular sarcomere lengthening.
Ventricle 1. The aggregate shortening of the sarcomeres in the layers of cardiac myocytes results in wall tension that leads to ejection of blood into the aorta and pulmonary artery PA. The active range of sarcomere length is only 1. Falling below 1. The collagen fiber network inhibits the stretching of sarcomeres much above 2. This integration of structure and function is important in permitting survival. If there were no skeleton, overstretch would lead to reduced emptying that would lead to more overstretch and no cardiac output CO.
Preload and compliance 1. Preload a. Where clinicians speak of preload, muscle physiologists think of sarcomere length. Compliance, a variable that can be dynamic, relates pressure and length. Measuring sarcomere length is essentially impossible clinically. As a surrogate indirect estimate of sarcomere length, clinicians measure a chamber pressure during chamber diastole.
Cardiovascular Concerns in Urosurgical Procedures Chapter Cardiovascular Concerns in Plastic Surgeries Chapter Cardiac Disease and Liver Surgery Chapter Oxford Cardiovascular Medicine. If the link is not responding kindly inform us through comment section. We will fixed it soon. We highly encourage our visitors to purch ase orig inal books from the respected publishers. If someone with copyrights wants us to remove this content, please contact us. Moreover Medstudentscorner. If you feel that we have violated your copyrights, then please contact us immediately.
Your email address will not be published. Save my name, email, and website in this browser for the next time I comment. For instance, the chapter on postoperative care of the cardiac patient contains extremely brief discussions of tamponade and pneumothorax. However, these topics are covered in detail in the chapter devoted to cardiothoracic emergencies. Similarly, the chapter on cardiac transplantation does not mention heart—lung transplants, a topic later discussed in a chapter about anesthesia for lung surgery.
Although this book is not designed to compare with other authoritative texts, such those edited by Kaplan and Thys, it is still a valuable resource both for trainees and practicing clinicians.
Many chapters, such as those discussing electrophysiology and pacing, congenital heart disease, the pathophysiology of cardiopulmonary bypass, and cardiac transplantation, are quite comprehensive. Numerous recent references and the number of prominent contributing authors lend credibility to the text.
A Practical Approach to Cardiac Anesthesia, 3rd Edition , compares favorably with other similarly sized volumes i. Stamford, Connecticut, Appleton and Lange, , especially in its discussion of anesthesia and analgesia for thoracic surgery. In conclusion, I would recommend this book as a thorough yet readable text for the anesthesia trainee and as a quick reference for the practicing anesthesiologist. Sign In or Create an Account. Advanced Search. Sign In. Skip Nav Destination Article Navigation.
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