Anesthesia for Veterinary Technicians

Susan Bryant

• Publisher: Wiley-Blackwell
• Year: 2013
• Print ISBN: 9780813805863
• eBook ISBN: 9781118692219
• Edition: 1
• Topic: Medicine
• Subtopic: Veterinary Medicine

Anesthesia for Veterinary Technicians is a highly practical guide to anesthesia skills for veterinary technicians published in association with the Academy of Veterinary Technician Anesthetists (AVTA). Packed with hints and tips to aid technicians in the practice of veterinary anesthesia, the book offers an essential resource to building anesthesia skills and improving knowledge. Encompassing both background knowledge and practical application of anesthesia-related skills, Anesthesia for Veterinary Technicians is a valuable resource for veterinary technicians of all skill levels.

Supplementary website materials, including charts and forms for use in the practice, are available at www.wiley.com/go/bryant.

1

Review of Cardiovascular and Respiratory Physiology

Susan Bryant

Most anesthetic drugs affect the cardiovascular and/or pulmonary systems in some way. It is important for the anesthetist to have at least a basic understanding of how these systems function and what impact anesthetic drugs are likely to have on them. This chapter reviews the basic physiology of the cardiovascular and respiratory systems, and some of the terminology related to them, as they relate to anesthesia.

The Cardiovascular System

Anatomy and physiology of the heart

The cardiovascular system consists of the heart, which is a muscular pumping device, and a closed system of vessels: the arteries, veins, and capillaries. The heart is responsible for pumping blood around the body, carrying nutrients to all parts of the body, and carrying waste away for removal. The heart consists of four chambers: the right atrium, the right ventricle, the left atrium, and the left ventricle. Arteries are the vessels that carry blood from the heart, and veins carry blood to the heart. Sodium, chloride, potassium, and calcium are the electrolytes that are most important for normal cardiac function. Depolarization of the cell occurs when sodium channels in the cell membrane open increasing sodium permeability. Resting membrane potential becomes less negative due to an influx of positive sodium ions. Cells begin repolarizing when the sodium gates close and negatively charged chloride ions begin to move into the cell. This causes calcium channels to open, allowing an influx of these ions. Final repolarization occurs when the calcium channels close and potassium permeability increases. Any alterations of normal plasma concentrations of these electrolytes can affect cardiac muscle function.

The sino-atrial (SA) node in the wall of the right atrium initiates the heartbeat. Impulses from this node transmit to the atrioventricular (AV) node. Other impulses in the heart are transmitted by the bundle of HIS, the bundle branches, and the purkinje fibers. Any damage to the cardiac muscle can result in unsynchronized impulse transmission, irregular heart contractions, and reduced cardiac output. The SA node acts as an intrinsic pacemaker and controls the rate of contractions. Both parasympathetic and sympathetic nervous systems innervate the SA node. Acetylcholine and noradrenaline are nervous system mediators that affect sodium, calcium, and potassium channels and can increase or decrease depolarization. Many drugs used for anesthesia purposes can affect heart rate, and therefore monitoring is strongly indicated.

Cardiac cycle

The cardiac cycle is the complete series of events that happens in the heart during one heartbeat. Blood flows into the atria from the vena cava and pulmonary veins. The cycle starts with depolarization at the SA node leading to atrial contraction. The atrioventricular valves, called the mitral and tricuspid valves, open when atrial pressure exceeds ventricular pressure. While the atria contract, blood flows into the relaxed ventricles. This is diastole, when the ventricles are relaxed and filling. Next, the atria relax and the ventricles contract (systole) pushing blood out the aortic and pulmonary valves. Ventricular systole causes closure of the atrioventricular valves and this action is the first heart sound heard on auscultation. The second heart sound is generated when ventricular relaxation occurs and the pulmonic and aortic valves close. Murmurs are abnormal cardiac sounds and usually result from malfunction of the valves (Reece 1997).

Electrical activity

As the heart undergoes depolarization and repolarization, the electrical currents that are generated (as described above) spread not only within the heart, but also throughout the body. This electrical activity generated by the heart can be measured by electrodes placed on the body surface. The recorded tracing of this activity is called an electrocardiogram (ECG or EKG). The different waves that comprise the ECG represent the sequence of depolarization and repolarization of the atria and ventricles. The complete cardiac cycle that is portrayed on the ECG is represented by waves that are identified as P wave, QRS complex, T wave.

The P wave represents the wave of depolarization that spreads from the SA node throughout the atria. The brief isoelectric period after the P wave represents the time in which the impulse is traveling within the AV node and the bundle of HIS. The period of time from the onset of the P wave to the beginning of the QRS complex is termed the P-R interval. This represents the time between the onset of atrial depolarization and the onset of ventricular depolarization. If the interval is prolonged or no QRS complex follows (the impulse is unable to be conducted to the ventricles), there is an AV conduction block (1st, 2nd, or 3rd degree AV block).

The QRS complex represents the ventricular depolarization. The duration of the QRS complex is normally of relatively short duration, which indicates that ventricular depolarization occurs very rapidly. If the QRS complex is prolonged, conduction is impaired within the ventricles. This can occur with bundle branch blocks or whenever an abnormal pacemaker site becomes the pacemaker driving the ventricle. Changes in the height and width of the QRS complex can indicate left heart enlargement. The shape of the QRS complex can also change depending on placement of the electrodes. The isoelectric period following the QRS (ST segment) is the time at which the entire ventricle is depolarized. The ST segment is important in the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated.

The T wave represents ventricular repolarization and is longer in duration than depolarization. The Q-T interval represents the time for both ventricular depolarization and repolarization to occur and therefore roughly estimates the duration of an average ventricular action potential. At high heart rates, ventricular action potentials shorten in duration, which increases the Q-T interval. Prolonged Q-T intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias.

Determining heart rate from an ECG strip

Heart rate can be determined by examining an ECG rhythm strip. The ventricular rate can be determined by measuring the time intervals between the QRS complexes, which is done by looking at the R-R intervals. Assuming a recording speed of 25 mm/sec and a lead II ECG, one method is to divide 1500 by the number of small squares on the recording paper between two R waves. Or one can divide 300 by the number of large squares between waves (Blaze and Glowaski 2004). If the heart rate is irregular, it is important to determine a time-averaged rate over a longer interval. Changes in heart rate can affect the function of the heart. Very fast heart rates can reduce cardiac output by not allowing the ventricles to fill adequately (Clark 2003). Bradycardia can also affect cardiac output. Troubleshooting heart rate abnormalities should include identifying and correcting the underlying cause if possible. Treatment with fluid therapy and/or additional analgesics may be necessary for tachycardic patients. Lightening anesthetic depth and/or treatment with an anticholinergic may be necessary for bradycardic patients. Arrhythmias should be identified and their effect on cardiovascular function should be determined before treatment therapy is decided on.

Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length. It is also referred to as inotropism. Preload is the force acting on a muscle just before contraction, and it is dependent on ventricular filling (or end diastolic volume). Preload is related to right atrial pressure. The most important determining factor for preload is venous return. Hypovolemia, vasodilation, and venous occlusion decrease preload.

Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure; afterload for the right ventricle is determined by pulmonary artery pressure.

Blood pressure is the driving force for blood flow (perfusion) through capillaries that supply oxygen to organs and tissue beds of the body. Blood pressure is needed to propel blood through high-resistance vascular beds, including those of the brain, heart, lungs, and kidneys. Blood pressure variations are detected by baroreceptors that are present throughout the cardiovascular system. These baroreceptors are capable of stimulating the autonomic nervous system in response to increases and decreases in blood pressure. If blood pressure falls, the sympathetic nervous system is stimulated and outflow will be increased, causing an increase in heart rate and blood pressure. If blood pressure increases, the parasympathetic system works to slow the heart rate and decrease pressure (Fraser 2003).

Blood pressure values are expressed in millimeters of mercury (mm Hg) and as three measurements: systolic, mean, and diastolic. Remember that the systolic pressure is the pressure generated when the left ventricle is fully contracted. Diastolic pressure is the pressure measured when the left ventricle relaxes. Pulse pressure felt on peripheral arteries is the difference between the two numbers. Mean arterial pressure (MAP) is calculated as diastolic pressure + 1/3 systolic pressure (systolic pressure − diastolic pressure) (Smith 2002). Mean blood pressure determines the average rate at which blood flows through the systemic vessels. It is closer to diastolic than to systolic because, during each pressure cycle, the pressure usually remains at systolic levels for a shorter time than at diastolic levels. Most times, under anesthesia, a patient’s mean pressure is what the anesthetist focuses on. A mean arterial pressure of at least 60 mm Hg (70 in horses) is needed to properly perfuse the heart, brain, and kidneys. Mean arterial blood pressures consistently below 60 mm Hg can lead to renal failure, decreased hepatic metabolism of drugs, worsening of hypoxemia, delayed recovery from anesthesia, neuromuscular complications, and central nervous system abnormalities, including blindness after anesthesia (Smith 2002). Prolonged hypotension (> than 15–30 minutes) can lead to nephron damage. Although the effects may not be immediately apparent because 65–75% of nephrons need to be damaged before renal disease becomes clinically observable, the effects may play a role in the onset of renal disease later in a pet’s life. Severe untreated hypotension can lead to cardiac and respiratory arrest. Hypertension, or excessively high blood pressure, can lead to problems as well. Ideally, any animal under anesthesia should have should have regular blood pressure monitoring because most anesthetic drugs affect blood pressure in some way.

Mean arterial blood pressure (MAP) = cardiac output (CO) × systemic vascular resistance (SVR). Cardiac output is defined as the amount of blood pumped by the heart in a unit period of time. Cardiac output is a term that is often used in anesthesia because it is extremely important in the overall function of the cardiovascular system. In general, the term applies to how well the cardiovascular pump (heart) is working. Many factors affect CO, directly or indirectly, including some anesthesia drugs. CO = heart rate (HR) × stroke volume (SV). Contractility is the amount of force and velocity that the ventricles can exert to eject the volume within them (Hamlin 2000). Systemic vascular resistance is the amount of resistance to flow through the vessels. Some vessels may be dilated and therefore allow more flow at less resistance. Constriction of vessels may limit blood flow and require more pressure to get blood through. It’s important to know that many of the drugs used for anesthesia affect one or more of these systems in some way.

Normal systolic blood pressures in the conscious awake patient are 100–160 mm Hg, normal diastolic pressures are 60–100 mm Hg, and normal mean arterial blood pressure ranges are 80–120 mm Hg. Hypotension is classified as MAP of less than 60 mm Hg. It is important to be able to identify the cause of a blood pressure abnormality to know how to begin treatment for it. There are generally three things to consider when looking for causes of hypotension. Look for drugs or physiological/pathological factors that may reduce systemic vascular resistance (SVR), look at heart rate, and look for things that affect stroke volume (preload/contractility) (Smith 2002). As mentioned earlier, many of the drugs used in anesthesia cause some degree of hypotension, and less often, hypertension. Knowing the side effects of these drugs and how they work will help in determining treatment. Drugs that decrease SVR (and cause vasodilation) in a dose-dependent manner include acepromazine, thiobarbiturates, propofol, and the inhalants. Other physiologic factors that may cause a decrease in blood volume or vascular tone include hemorrhage, inadequate volume administration or replacement, dehydration, shock, sepsis, anaphylaxis, or severe hypercapnia (high CO₂) (Smith 2002). Patients with acid/base abnormalities should be stabilized prior to anesthesia if possible to help reduce the possibility of hypotension. Drugs that can decrease heart rate include opioids, alpha 2 agonists, and the inhalant drugs isoflurane and sevoflurane. Patients with intracranial disease, hypothermic patients, and extremely fit pets may have low heart rates (bradycardia). Anesthetic drugs affecting the contractility of the heart include the inhalants, thiobarbiturates, propofol, and alpha-2 agonists. The inhalant drugs are potent vasodilators, with up to a 50% reduction in cardiac contractility at surgical planes of anesthesia as well. The other drugs’ effects on contractility are more transient and less profound. Alpha-2 agonists and phenylephrine cause vasoconstriction of blood vessels, which results in hypertension. The effects of hypertension from the alpha-2 agonists are transient, lasting only a few minutes before the vessels relax and hypotension can result. The dissociative drugs, ketamine and Telazol, have indirect positive effects on the cardiovascular system and thus increase heart rate, but this can cause a reduction in stroke volume depending on how severely heart rate is affected. Patient positioning can affect blood pressure. Obese or bloated patients or patients with large abdominal masses placed in dorsal recumbency may be hypotensive due to excessive pressure on the caudal vena cava. This pressure may compromise venous return and result in hypotension. The same can happen when positive pressure ventilation is used.

Certain disease states can cause hypertension, including renal disease, pheochromocytomas, pulmonic stenosis, heartworm disease, and hyperthyroidism. Ideally, these patients will have their hypertension well controlled before surgery. The exception may be the pheochromocytoma patient whose hypertension may spike up during surgery when the tumor is manipulated. A nitroprusside CRI may be indicated for these patients if systolic pressure exceeds 200 mm Hg. If a patient develops hypertension under anesthesia that is not related to a disease state, the cause is most likely related to inadequate anesthetic depth and/or inadequate analgesic administration. Adjusting anesthetic depth and providing additional pain medications should result in normotension.

Changes in blood volume ...

Table of contents

• Cover
• Contents
• Title Page
• Copyright
• Contributors
• Preface
• Acknowledgements
• 1. Review of Cardiovascular and Respiratory Physiology
• 2. The Preanesthetic Workup
• 3. Mathematics and Calculations for the Veterinary Anesthetist
• 4. Records and Record Keeping
• 5. Preanesthetic Preparation
• 6. Intravenous Access
• 7. Airway Maintenance
• 8. Anesthesia Equipment
• 9. Introduction to Monitoring: Monitoring the ECG and Blood Gases
• 10. Monitoring: Pulse Oximetry and Temperature, and Hands-On
• 11. Monitoring Blood Pressure and End-Tidal CO2 in the Anesthetized Patient
• 12. Fluid Therapy and Blood Products
• 13. Premedication and Sedation Drugs
• 14. Induction Drugs
• 15. Inhalant Anesthetics
• 16. Recovery of the Anesthetic Patient
• 17. Anesthetic Complications and Emergencies
• 18. Ventilation Techniques in Small Animal Patients
• 19. Anesthesia for Ophthalmology Patients
• 20. Anesthesia for Patients with Cardiac Disease
• 21. Anesthesia for Small Animal Patients with Head Trauma or Increased Intracranial Pressure
• 22. Anesthesia for Thoracotomies and Respiratory-Challenged Patients
• 23. Anesthesia for Patients with Endocrine Disease
• 24. Anesthesia for Patients with Renal Disease
• 25. Anesthesia for Patients with Liver Disease
• 26. Anesthesia for Pediatric Patients
• 27. Anesthesia for Geriatric Patients
• 28. Cesarean Section Techniques
• 29. Anesthesia for Emergency Trauma Patients
• 30. Anesthesia for Nontrauma Emergency Patients
• 31. Anesthesia for Small Exotics: Ferrets, Rodents, and Rabbits
• 32. Basic Physiology of Pain
• 33. Pain Assessment
• 34. Pain Management Strategies
• 35. Equine Anesthesia
• 36. Ruminant Anesthesia
• Index