Basic Monitoring in Canine and Feline Emergency Patients
eBook - ePub

Basic Monitoring in Canine and Feline Emergency Patients

Elizabeth J Thomovsky, Paula A Johnson, Aimee C Brooks, Elizabeth J Thomovsky, Paula A Johnson, Aimee C Brooks

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  1. 256 pagine
  2. English
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eBook - ePub

Basic Monitoring in Canine and Feline Emergency Patients

Elizabeth J Thomovsky, Paula A Johnson, Aimee C Brooks, Elizabeth J Thomovsky, Paula A Johnson, Aimee C Brooks

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This book discusses basic monitoring techniques that can be easily performed on emergency canine and feline patients in both first line emergency and primary care clinics. Techniques include blood pressure measurement, capnography, electrocardiography, pulse oximetry, and point of care monitoring ranging from the physical exam to bedside ultrasound and diagnostic tests such as PCV/TP, blood glucose and lactate.Each chapter begins with basic physiology as related to the monitoring technique, before reviewing how the piece of equipment used for monitoring works, pros and cons of the equipment, and limitations of the device. A simple, consistent layout for each chapter makes it easy to quickly locate information within the book. A final section in each chapter gives practical examples of how to use the monitoring technique in a clinical setting. The book also: - Emphasizes how physiology ties into what information each technique does (and does not) provide;- Includes pictures, tables, and diagrams to help explain concepts;- Delivers guidelines for rational interpretation of the results acquired. An important resource for both veterinary practitioners and students, this book provides a succinct approach to understanding the monitoring equipment used in emergency patients.

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Informazioni

Anno
2020
ISBN
9781789243017
Argomento
Medicine
1 Physical Examination and Point-of-care Testing
PAULA A. JOHNSON*
Purdue University College of Veterinary Medicine, West Lafayette, Indiana, USA
*Corresponding author: [email protected]
The efficient, accurate, and timely assessment of emergent patients is necessary to have successful outcomes. This chapter will review physical examination (PE) and point-of-care blood testing (POCT), important first-line tools that guide therapeutic decision making in an emergency and critical care setting. The specific point-of-care tests to be covered include packed cell volume/total protein (PCV/TP), blood glucose (BG), ketone values, and blood lactate. Point-of-care instrumentation is available, which also reports such parameters as electrolytes, blood gas values, acid–base, and coagulation. Discussion of these parameters as well as other point-of-care assessments, including blood pressure and point-of-care ultrasound, are covered elsewhere in this book.

1.1 Basic Physiology and Anatomy

Physical examination

As technology has evolved, more diagnostic instrumentation that allows for quick or instantaneous test results is readily accessible; as a result, the physical exam has seemingly decreased in its importance and utility. However, no technology can replace the value of the physical exam, defined as ‘an examination of the bodily functions and condition of an individual,’ for the practicing clinician. The physical exam is a skill that has to be nurtured, practiced, and fine-tuned by repetition and experience over time. In fact, the more experienced the clinician, the more important the information that can be gleaned from the exam. The benefits associated with performing thorough physical exams are numerous. Those benefits include its immediate availability, use of basic senses (seeing, hearing, touching, and smelling), and, with the exception of a stethoscope, lack of need for any special instrumentation. Additionally, it is cost-effective, provides a wealth of information regarding the patient’s clinical status in a short period of time, and can be utilized for serial monitoring to identify changes or trends in a patient’s condition or response to therapy.

Point-of-care blood testing

Blood glucose

As the primary source of fuel for energy production in most cells in the body, the availability and regulation of glucose is necessary to sustain life. In most cases, glucose is present in ample amounts in mammals although sometimes the ability to deliver the glucose to the needed locations can be challenging. An example would be a diabetic patient who has ample circulating glucose but is unable to provide that glucose to the mitochondria within the cells.
The concentration of glucose within the body is controlled within a set range during the resting state. Table 1.1 lists the reference range for BG in canines and felines at rest. Normal BG levels are primarily maintained by the hormone insulin that serves to transport glucose into the cells for conversion to adenosine triphosphate (ATP) by the stages of aerobic metabolism (glycolysis, transport through the tricarboxylic [TCA] cycle, and passage through the electron transport chain). Thus, insulin’s major effect is to lower the BG concentration. BG levels are further regulated and the effects of insulin opposed by the counter-regulatory hormones glucagon, cortisol, epinephrine, and growth hormone. These hormones can stimulate further glucose release into the bloodstream to maintain or increase BG levels. When glucose is not maintained under tight control, hypoglycemia or hyperglycemia can occur. Both conditions can be affiliated with morbidity and mortality.
Table 1.1. Normal reference range for blood glucose during the resting state in dogs and cats.
Species
Normal reference range (mg/dL)
Canine
80–120
Feline
80–140
The brain is an obligate glucose user and has reduced or minimal capabilities to liberate its own glucose from glycogen stores or to use protein as an energy source. Therefore, the brain relies on systemic delivery of glucose to maintain normal metabolic function. Thus, when hypoglycemia occurs, not only are the majority of clinical signs associated with insufficient glucose delivery to the brain (neuroglycopenia), but they also occur within a relatively short period of time. If the hypoglycemia is not corrected quickly or is allowed to persist for an extended period of time, these neurologic-related clinical signs may persist beyond the time of correction and may progress to include cortical blindness and peripheral nerve demyelination.
Hyperglycemia can be tolerated for longer periods of time with the more minor increases in BG (<200 mg/dL) typically not leading to clinical signs and hence able to be tolerated for longer periods of time. Severe hyperglycemia (>200 mg/dL) is associated with clinical signs and is not tolerated for long periods. The most common clinical signs in the case of hyperglycemia are associated with fluid losses. This is due to the fact that significant hyperglycemia causes fluid to shift into the vascular space from the cells. Large quantities of glucose molecules act as an effective osmole and draw water from the cells into the vasculature. These fluid shifts lead to cellular dehydration. At the same time, the glucose molecule will similarly retain water with it in the renal tubules, leading to polyuria. Significant polyuria can cause enough fluid and concurrent electrolyte loss via the urinary system to lead to further cellular dehydration and electrolyte deficiencies (especially hypokalemia and hyponatremia). Typically, glucosuria (and volume loss through the kidneys) starts to occur in dogs and cats when the serum glucose exceeds 180–200 mg/dL and 260–310 mg/dL, respectively. Hyperglycemia has also been linked to other deleterious consequences such as immunosuppression, increased inflammation, disruption of normal coagulation, and alterations of the endothelium.

Ketone levels

Ketones are produced as a consequence of fat store metabolism. While ketosis can occur with other disease states such as hepatic lipidosis, starvation, or errors of metabolism, the most common situation in veterinary patients in which measurement of ketones is important is in patients suspected or known to have diabetes mellitus. Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus marked by hyperglycemia with excessive ketone production and subsequent acidosis from the ketones. In DKA, a lack of insulin production and/or lack of insulin binding to its receptors on cells coupled with an increase in counter-regulatory hormones including glucagon, epinephrine, glucocorticoids, and growth hormone leads to an increase in glucose levels within the bloodstream. In addition, free fatty acid (FFA) breakdown increases in response to the counter-regulatory hormones in an attempt to create more glucose and provide more energy to the cells. The excessive amount of FFAs presented to the cells overwhelm their ability to oxidize these FFAs to acetyl coenzyme A to enter the TCA cycle and undergo aerobic metabolism to ATP. Instead, the excess FFAs are oxidized to ketone bodies that are released into the circulation.
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