THE UPS AND DOWNS OF THE ECG COMMON ARRHYTHMIAS IN THE ICU Elke Rudloff, DVM, DACVECC www.lakeshorevetspecialists.com Cardiac function relies on a specialized excitation and conduction system of cardiac muscle and a coordinated contractile process. Alterations of the stimulating nodes, conduction pathway, and myocardial fibers can affect rhythmicity and efficacy of the pump system. Conditions often encountered in the critically ill animal (hypoxia, ischemia, electrolyte imbalances, neuromuscular disease, inflammation, toxemia, medications, etc.) can affect the conduction system, resulting in incomplete or abnormal conduction pathways, chaotic cardiac muscle contraction, and reduced cardiac output and tissue perfusion. With the severest dysrhythmias, cardiac arrest can occur. Electrocardiogram (ECG) interpretation is required to characterize a cardiac dysrhythmia, as an adjunct to determining cardiac enlargement, and as an indicator for certain electrolyte, systemic, and metabolic disorders. Treatment of dysrhythmias will be based on the ECG diagnosis and cardiovascular status of the patient. An aberrant conduction of an electrical impulse through the heart (dysrhythmia; arrhythmia) can occur independently and myocardial disease is not required. Arrhythmias must be distinguished from 60cycling activity and artifact from improperly placed leads, or patient movement. Good contact must be made between the leads and the patient’s skin. Thick-haired dogs may need to have their hair clipped, and clean clips should be used with secure contacts. Electrode pads can be placed for continuous monitoring, or on the bottom of the digital pads. Contact is enhanced with electrode cream or alcohol. Alcohol should never be used when electrocautery use or defibrillation is anticipated. Arrhythmias are identified by their rate followed by the types of aberrant impulses and by their anatomic origin. Tachyarrhythmias Sinus tachycardia Atrial fibrillation Bradyarrhythmias Sinus bradycardia SA standstill Normal Rates Sinus arrhythmia Junctional rhythm 1st degree AV block
Junctional tachycardia Atrial flutter
Ventricular tachycardia Atrial standstill
Junctional escape 3rd degree AV block
Ventricular escape Sinus arrest
Sinus arrest Atrial premature beat 2nd degree AV block
Accelerated idioventricular rhythm Ventricular premature beat Bundle branch block
SINOATRIAL ARRHYTHMIAS: a p-wave associated with each normal qrs complex. Sinus arrhythmia: r-r intervals are different, but are associated with respiration (and the vagal influence of respiration). Sinus block: the r-r intervals will occasionally be double the normal length, p-qrs-t complexes are normal. Sinus arrest: the r-r interval is periodically longer than double the normal length. Sinus tachycardia: the heart rate is increased (in our hospital we consider this >140 bpm in the dog and >200 bpm in the cat).
Sinus bradycardia: the heart rate is decreased (in our hospital we consider this <70 bpm in the dog and <150 bpm in the cat).
ATRIAL FIBRILLATION: p-waves are not normal, â&#x20AC;&#x153;fâ&#x20AC;? wave predominate (fibrillation of the atria), with normal qrs complex. The r-r interval is irregular and unpredictable. The qrs rate is generally fast, however slow afib can occur.
SUPRAVENTRICULAR FOCI Atrial premature beats: The primary rhythm is a sinus rhythm, with an occasional p-qrs complex that discharges earlier than expected. The qrs of the APC is like the normal beats, but the p-wave and the p-r interval may be different.
Atrial tachycardia: Paroxysms of tachycardia where the p-wave and p-r interval are different than the normal beat. The r-r intervals of the burst are consistent.
JUNCTIONAL FOCI Junctional escape rhythm: Impulse originates from the AV node producing the qrs impulse that appears normal. The p-wave can occur before, during or after the qrs wave, and may be negative. The rate is slower than the sinus node.
Junctional tachycardia: p-waves are negatively deflected in the Lead II with normal qrs complexes. The rate is >150bpm. VENTICULAR FOCI Ventricular premature contraction: The primary rhythm is a sinus rhythm, and intermittent ventricular premature contractions (VPC) occur. The abnormal contraction is wide and bizarre, and not associated with any p-wave. There may be a pulse deficit associated with the contraction. When multiform VPCâ&#x20AC;&#x2122;s exist, there is a greater chance for ventricular tachycardia and fibrillation.
Ventricular tachycardia: The primary rhythm is ventricular with rates >100bpm. There are no associated pwaves with the qrs complexes, and the qrs complexes are wide and bizarre.
Ventricular flutter: Structure to the qrs wave is lost, and this rhythm can rapidly lead to ventricular fibrillation.
Ventricular fibrillation: No discernable p-qrs complexes, this rhythm appears as baseline undulations. There is no heart beat or pulse associated with this rhythm.
Escape beat: The primary rhythm is a wide and bizarre qrs with no p-wave, which occurs during bradycardia lasting long enough for the ventricular pacemaker to discharge. An escape rhythm occurs when the beat predominates. Idioventricular rhythm: A slow, regular ventricular rhythm.
Accelerated idioventricular rhythm: An idioventricular rhythm under autonomic influence that breaks through a sinus rhythm at a slightly faster rate than the sinus rate. Typically, it emerges when a respiratory sinus arrhythmia slows down during inhalation and disappears when the rate increases again during exhalation. There are no perfusion abnormalities associated with the rhythm and it requires no treatment.
CAPTURE BEAT: The normal beat that emerges within a series of ventricular beat.
FUSION BEAT: Combination of a VPC and a normal beat, usually occurring between a VPC and normal beat.
CONDUCTION DISTURBANCES: alter the appearance of the waves and are caused by delays or blockages of the electrical pathway, chamber enlargement, and pericardial effusion. 1st degree AV Block: The rate and rhythm is normal with a constant p-qrs configuration; however, the p-r interval is >0.13s in the dog and 0.09s in the cat. 2nd degree AV Block: Occurs when a beat is missed or abruptly dropped. Mobitz Type I has a prolonged p-r interval just prior to the dropped qrs. Mobitz Type II has a normal p-r prior to the dropped qrs.
3rd degree AV Block: No association between the p-wave and the qrs. There is a complete block of the SA impulse at the AV node, and automaticity of the sub-AV system kicks in.
Sinoatrial standstill: Absence of p-waves, primary junctional or ventricular rhythm. Bundle branch blocks: Widening of a positive qrs >0.07s is suggestive of a left origin BBB and wide and deep s-wave with right origin BBB. LBBB is usually associated with heart disease. Wolf-Parkinson-White syndrome: Conduction goes from atria directly to the ventricles through a different conduction path and bypasses AV node. P-QRS are constant, P-R less than 0.06 sec, QRS prolonged.
Electrical alternans: Alternating r-wave amplitudes. This suggests excessive movement of the heart, and is associated with pericardial effusion.
Pulseless electrical activity: An electrical impulse that is generated without myocardial contraction. This complex can appear as a p-qrs, or wide and bizarre qrs, identified by a very slow rate (generally < 60bpm). Indicates cardiac arrest.
ANTIARRHYTHMIC TREATMENT Antiarrhythmic medications have the potential for inducing arrhythmias, or worsening arrhythmias. Treatment of arrhythmias is indicated to alleviate cardiovascular compromise, reduce the risk for potentially life-threatening arrhythmias, and to reduce the risk of myocardial damage. Oxygen is administered. Electrolyte imbalances, severe acidemia, hypoxemia, hypoglycemia and exposure to drugs/toxins that affect myocardial function are immediately addressed. It is not unusual for ventricular arrhythmias in the dog to be associated with abdominal organ dysfunction such as hepatic or splenic masses. Hyperthyroidism should be investigated for when an older cat presents with a tachycardia. Supraventricular tachyarrhythmias (SVT) may be manipulated by inducing a vagal maneuver. For acute therapy, IV calcium channel blockers and beta blockers may be used. Life-threatening refractory SVT may be treated with adenosine, digoxin, phenylephrine or edrophonium. Chronic therapy may include oral digoxin +/- beta-blocker or calcium channel blocker. Ventricular tachyarrhythmias (VT) are generally not treated unless they are electrically unstable or promote hemodynamic instability. Examples include multiform complexes, r on t phenomenon, rapid tachycardia (>180-200 bpm). In acute situations lidocaine is administered IV. Additional medication may include IV procainamide, amiodarone, esmolol or sotalol. Chronic therapy may include treatment with oral sotalol, atenolol, mexiletine, or procainamide. Symptomatic bradyarrhythmia can be immediately treated with anticholinergics (atropine or glycopyrrolate), but may require pacemaker implantation.
Hypoglycemic Crisis Elke Rudloff, DVM, DACVECC Lakeshore Veterinary Specialists Glucose is the main molecular source of adenosine triphosphate (ATP) production that all cells in every organ require to exist. The brain, almost exclusively, uses glucose for energy (it uses 25% of all glucose in the body), but cannot synthesize or store it. It has 3 times the metabolic rate than other tissues, is the most susceptible to hypoglycemia. Glucosensing neurons in the ventromedial hypothalamus trigger a sympathoadrenal response to hypoglycemia. The release of epinephrine, glucocorticoid, and glucagon suppresses endogenous insulin secretion, antagonizes insulin, and this process, along with the release of growth hormone, increases the production and release of glucose. This increases circulating glucose levels and maintains a glucose supply for neuronal cells, which do not require insulin for glucose uptake. Hypoglycemia is a life-threatening condition that, untreated, can result in neurologic injury, cardiovascular collapse, and death. The neuroendocrine response to hypoglycemia can manifest in clinical signs, such as nervousness, tremors, and weakness. These clinical signs are reported to occur in normal animals when plasma glucose levels approach 64.8â&#x20AC;&#x201C;68.4 mg/dL. Untreated hypoglycemia will result in neuroglycopenia, a syndrome in which hypoglycemia results in neurologic signs. When protracted or severe, hypoglycemia exhausts counterregulatory mechanisms, and excitotoxin (e.g. glutamate, aspartate) release, apoptosis, and pseudolaminar necrosis can occur in the brain. In addition, cardiac and respiratory arrest can occur. The rapidity and degree of hypoglycemia determine the severity of clinical signs. Treatment and Testing The most reliable criteria for diagnosing clinically significant hypoglycemia are: (1) clinical signs of hypoglycemia, (2) blood glucose <60 mg/dL, and (3) relief of signs after glucose supplementation. When neurological signs are apparent and hypoglycemia a consideration, it is ideal to document the blood glucose level. Handheld glucometers allow easy and quick determination of blood glucose levels using minimal blood. However, very low blood glucose levels can fail to generate a reading, and falsely low readings can occur when serum is hemoconcentrated, testing is delayed, or serum is not separated from glucose-consuming blood cells. Dry chemistry analyzers provide more consistent results when serum or plasma has been separated from red cells and the sample is immediately evaluated. A comprehensive evaluation into the cause of hypoglycemia may include a complete blood count, serum biochemical profile, urinalysis, urine culture and susceptibility, thoracic radiography, abdominal ultrasonography, blood insulin:glucose ratio, ACTH stimulation, and pre- and post-prandial bile acids. Figure 2 outlines the interventions for hypoglycemia. If IV access is not readily available, a dextrose gel, Insta-Glucose (Valeant Pharmaceuticals, Aliso Viejo, CA), can be rubbed on the oral mucous membranes, where it is directly absorbed and immediately available. Corn syrup contains fructose and can also be rubbed on the gums for absorption, but it requires hepatic metabolism to dextrose. Owners of pets at risk for hypoglycemia should keep these products available for immediate administration. When IV access exists, a bolus of 1 mL/kg of 25% dextrose in normal saline (or 0.5 mL/kg of 50% dextrose diluted 1:1 in normal saline) is administered. Continuous dextrose supplementation is recommended until the cause of the hypoglycemia has been corrected or eliminated using a constantrate infusion of 1.25%â&#x20AC;&#x201C;10% dextrose in a replacement or maintenance solution. When the fluid rate is increased to replenish extracellular volume depletion, then 1.25% dextrose may be used. The blood glucose should be periodically monitored (within 30-60 minutes after any adjustment) until an accurate assessment can be made of the response to treatment. It is preferred to prevent over-supplementation since this can cause osmotic fluid shifts, diuresis and fluid loss. In the patient with a suspected insulinoma,
over-supplementation can stimulate release of endogenous insulin and drive the glucose level down further. Ultimately the desired glucose level is one that eliminates clinical signs, and is > 60 mg/dL. When dextrose solutions of 7% or greater are needed for prolonged periods, infusion via a central line reduces the risk of phlebitis. Glucagon (50 ng/kg/min IV or IM followed by then 5–40 ng/kg/min IV continuous infusion) is useful for hypoglycemic patients with adequate glycogen stores (e.g., insulin overdose, insulinoma) that have difficulties maintaining glucose levels with dextrose supplementation. Once clinical signs of hypoglycemia have abated and measures for glucose control have been instituted, the rate can be reduced and discontinued. Owners of diabetic pets can store and administer IM glucagon injections at home for emergency use before transport. Glucocorticoids can be used as a stop gap to increase blood glucose while definitive treatment of certain neoplastic disorders, such as insulinoma are in progress. Glucocorticoids increase hepatic gluconeogenesis and decrease glucose uptake by peripheral tissues by inhibiting insulin binding to their receptors. This increases glucose availability for neuronal tissue. Glucocorticoids are part of the definitive treatment for cortisol deficiency (naturally occurring or iatrogenic hypocortisolism). Glucocorticoid treatment can reduce diagnostic yield of certain steroid-responsive diseases, therefore obtaining samples for diagnostic evaluation prior to their initiation is ideal (e.g. blood samples for insulin levels, cytological/histopathological samples for neoplasia). The dose of prednisone can range from a physiologic dose to an anti-inflammatory dose (0.25–1 mg/kg IV or PO q12h). Initial treatment with dexamethasone (0.5–1 mg/kg IV or PO q 12h) is preferred if testing for hypocortisolism is anticipated or in progress to reduce false positive results which can occur with prednisone administration. If refractory seizures and altered mentation related to cerebral edema and neuronal injury persist despite normalization of blood glucose, mannitol (500–1000 mg/kg IV as a slow bolus over 20 minutes) may improve cerebral blood flow. If positive results are seen, the dose is repeated 2–3 times every 2 hours. Contraindications to mannitol infusion include fluid-intolerant states (e.g., heart disease, oliguric or anuric renal failure), hyperosmolar states (e.g., hypernatremia), and severe dehydration. Table 1: Causes and definitive therapy for hypoglycemia Cause Definitive Therapy Artifact (pseudohypoglycemia) Seizure Seizure control Counterregulatory hormone deficiency Hormone supplementation Decreased hepatic glycogen stores Nutritional therapy Hypocortisolism Glucocorticoid supplementation Infection Antimicrobial therapy, organ support Sepsis Virulent babesiosis Neoplasia Cancer treatment; glucocorticoids Insulinoma (pancreatic beta-islet cell tumor) Others Hepatic failure Nutritional therapy, symptomatic treatment Toxicity Symptomatic treatment Bread Dough Xylitol Insulin Sulfonylurea Beta-blockers
Strenuous exercise
Supplementation
Figure 1: Neurohormonal response to hypoglycemia. Glycogenolysis also occurs within the astrocyte. VMH, ventromedial hypothalamus; SNS, sympathetic nervous system; CBF, cerebral blood flow; GLUT, glucose transporters. (From Loose N, Rudloff E, Kirby R. Hypoglycemia and its effects on the brain. J Vet Emerg Crit Care 2008 18(3) 223-224.) Recommended Reading Feldman EC, Nelson RW. Beta cell neoplasia. Canine and Feline Endocrinology and Reproduction. 3rd Edition. (eds, Feldman EC, Nelson RW) Philadelphia: WB Saunders, 2004. pp 616-644. Todd JM, Powell LL. Xylitol intoxication associated with fulminate hepatic failure in a dog. J Vet Emerg Crit Care. 17(3):286-289, 2007. McMichael M, Dhupa N. Pediatric Critical Care Medicine: Specific Syndromes. Comp Cont Edu. 22 (4): 2000. Loose N, Rudloff E, Kirby R. Hypoglycemia and its effects on the brain. J Vet Emerg Crit Care 2008 18(3) 223-224. Koenig A. Hypoglycemia. Small Animal Critical Care Medicine, ed Silverstein D, Hopper K. 2009 Saunders Elsevier, St. Louis, MS. p295-299.
Figure 2: Interventions for hypoglycemia with and without neurological signs BG* < 60 mg/dL 3.33 mmol/L
No
Repeat test on plasma sample or dry chemistry
Neurological Signs? Yes
Yes
Yes
BG < 60 mg/dL 3.33 mmo/L
Glucometer Reading?
Yes
No
Glucose gel on gums IV Dextrose** + Dextrose CRI***
ď&#x201A; Meal frequency Decontaminate if toxin ingested Frequent monitoring for neurological signs
No BG < 60 mg/dL 3.33 mmol/L
Complete Blood Count, Serum Chemistry, Urinalysis Diagnostic Imaging Serum Insulin Bile acid testing Cortisol level and ACTH stimulation testing Fluid cultures
Yes
Glucagon Injection**** Consider corticosteroids
*BG: Blood glucose **1 ml/kg 25% dextrose ***CRI: Continuous rate infusion of 1.25-10% dextrose in normal saline **** 50 ng/kg/min IV/IM then 5-40 ng/kg/min IV
No
Evaluate for primary neurological disease
THE HYPOTENSIVE PATIENT WHAT TO DO WHEN FLUIDS DONâ&#x20AC;&#x2122;T WORKâ&#x20AC;Ś Elke Rudloff, DVM, DACVECC Lakeshore Veterinary Specialists, Glendale, WI Circulatory shock can be defined as a condition in which oxygenation of the tissues is inadequate to meet the metabolic demands of the cells. The most common cause of circulatory shock is inadequate intravascular volume, or hypovolemia because of loss of plasma water during vomiting and diarrhea or hemorrhage. A positive response to intravascular volume resuscitation is a hallmark indicator that hypovolemia is a cause of shock. What do you do when volume resuscitation is not effective at ameliorating the signs of shock? The objectives of this course are to review the pathophysiology of shock and causes of shock unrelated to intravascular volume depletion, and intervention. Cellular Homeostasis Energy is required for all metabolic functions of the cells and is stored in the high-energy bonds of adenosine triphosphate (ATP). When oxygen and glucose are available, aerobic energy production within the mitochondria results in the production of 38 ATP per glucose molecule. Tissues are unable to store oxygen making optimal ATP production dependent upon both oxygen delivery (DO2) to the tissues and oxygen utilization (VO2) by the mitochondria. As DO2 declines, anaerobic energy production will produce only 2 ATP per substrate molecule and lactic acid, which will be inadequate for anything other than a short period of inadequate DO2. Cardiovascular Contribution Oxygen is transported in the blood bound to hemoglobin and, to a minor extent, dissolved in the plasma of the blood. Delivery of oxygen to the tissues depends upon a bellows capable of supplying oxygen to the capillaries (respiratory system), a functional pump (heart), and a patent and dynamic conduit (blood vessels). The volume of blood ejected from the heart per minute (cardiac output) is the product of stroke volume (preload, afterload and contractility) and heart rate. Venous return (preload) increases the stretch of the heart chambers resulting in increased force of contraction. Factors influencing venous return to the heart include: mean circulatory filling pressures, right atrial pressures, and resistance of the arteries. Blood flow is also influenced by pressure differences and compliance within the vascular circuit as well as viscosity of the fluid medium. Extrinsic and intrinsic regulation of the cardiovascular system will also affect blood flow to the tissues. Intrinsic metabolic autoregulation affects local organ blood flow, and is influenced by oxygen availability and removal of metabolic byproducts. Extrinsic control is produced by a combination of hormonal and catecholamine influences. Should any of the above parameters function inadequately, cardiovascular and neuroendocrine compensatory mechanisms modify one or more component with the end goal of improving tissue perfusion. The heart and specific blood vessels are equipped with mechanoreceptors that identify the pressure within their walls. Physiologic adjustments are mediated through the stretch detecting baroreceptors that lie within the aortic arch and carotid sinuses. Afferent signals travel from these baroreceptors through the vagus (cranial nerve X) and glossopharyngeal (cranial nerve IX) nerves to the vasomotor center in the brain stem. When adequate pressure is detected, central excitatory, sympathetic efferent nerves are suppressed, and inhibitory, parasympathetic efferent nerves are enhanced, resulting in a normal heart rate and vascular tone. Sympathetic and parasympathetic receptors are stimulated by the neurotransmitters norepinephrine and acetylcholine, respectively. Additional receptors located in the atria and ventricles of the heart are sensitive to pressure and chemical changes. These receptors appear to play a key role in the distinctive triad of clinical signs seen in feline circulatory shock.
The cardiovascular response to a reduced effective circulating volume is initiated when a significant decline in cardiac output causes a decrease stretch of the vascular baroreceptors and cardiac mechanoreceptors. Afferent neurons stimulate the brainstem vasomotor center causing a sympathetic excitatory response and inhibition of the parasympathetic tone. This results in tachycardia, increased inotropy and mild vasoconstriction that can be sufficient in some patients to support tissue perfusion until the cause of the shock has been rectified. This phase is recognized clinically by tachycardia, bounding peripheral pulses, a rapid capillary refill time (CRT), and bright pink or red mucous membrane color (MM) and is called the compensatory stage of shock. This compensation is transient and requires large quantities of energy. While this stage is commonly recognized in dogs and humans, it may be very brief (minutes) in the cat and is rarely seen clinically. The cat in circulatory shock will demonstrate at least bradycardia and hypotension in the early stages with hypothermia developing as shock progresses. If volume replacement does not occur, or is inadequate, then peripheral vasoconstriction and tachycardia persist with selective vasoconstriction of the skin, mucous membranes, and splanchnic bed shunts arterial blood flow to preferred organs (i.e. heart and brain) to ensure basic life-support. Cellular oxygen and energy demands increase as vasoconstriction intensifies. Oxygen consumption becomes dependent on oxygen delivery, and anaerobic glycolysis results in lactic acid production. Other vasoactive substances produced due to local tissue hypoxia at the capillary level cause local vasodilatation and increased capillary permeability resulting in maldistribution of blood flow in the hypoxic tissue beds. When chemical mediators (cytokines) produced locally in hypoxic tissues enter the systemic circulation they incite a systemic inflammatory response syndrome (SIRS). Significant vasodilatation and damage at the endothelial lining resulting in increased capillary permeability further depletes intravascular volume. Redistribution of blood flow occurs, leading to further consequences. This multilevel cellular dysfunction places the animal in the early decompensatory (middle) stage of hypovolemic shock. Clinical signs of this stage in the dog include tachycardia, pale mucous membrane color, prolonged capillary refill time, and hypotension. Cats with hypovolemic shock will present with a sub normal temperature, decreased heart rate and a low arterial blood pressure. In the cat, the neuroendocrine response to hypovolemia appears to promote vasodilatation, hypothermia and bradycardia. Hypothermia can also lead to a poor response by the catecholamine receptors, augmenting vasodilatation and bradycardia. When intravascular volume loss is massive, when earlier compensatory responses are ineffective or inadequately treated, when the insult is severe and overwhelming, or when central pathology blunts the typical compensatory response, late decompensatory shock ensues. The cells are unable to meet the demands for ATP, manifesting in circulatory collapse and insufficient arterial flow to the brain and heart. The sympathetic center in the brain malfunctions, and the heart cannot sustain either a chronotropic or inotropic response. Clinical signs of this terminal stage are a result of organ failure: bradycardia, hypotension, no capillary refill time, white or cyanotic mucous membrane color, and anuria. Cardiopulmonary arrest is imminent without extreme supportive measures of compromised organs and aggressive cardiovascular resuscitation. The key to survival is aggressive resuscitation early in the shock process. Resuscitation from Hypovolemic Shock The goal is to deliver sufficient oxygen and substrate to the tissues for the cells to produce energy. Needed are intravascular volume to fill the vessels, a functioning pump, hemoglobin, oxygen supply, vascular tone, and an intact vasculature. Oxygen is administered by nasal catheter (0.1-0.2 L/kg/minute) or using a mask, hood, or clear bag. Single or multiple intravenous catheters are placed, and analgesia administered a needed. Control of external hemorrhage is initially accomplished by direct compression or bandaging. Vascular access is established and fluid administration initiated. Life-threatening intrathoracic or intraabdominal hemorrhage may require emergency surgical intervention for hemostasis.
The fluid therapy plan: The fluid therapy plan typically has a resuscitation, rehydration and maintenance phase. Resuscitation implies an urgent need to restore tissue perfusion and oxygenation. Because hypovolemia can be a significant component of most types of shock (even cardiogenic shock), the intravascular volume status must always be established. The type, quantity and rate of fluid administration required to reach the desired resuscitation end-points are determined and will depend on the type of shock and underlying conditions (Tables 1, 2, and 3). Additional circulatory support: The most common cause of non-responsive shock is inadequate volume (inadequate preload), either not enough fluid has been administered or volume losses are exceeding volume administered. Indirect indicators of preload include palpation of the jugular vein, measuring central venous pressure (CVP), and ultrasonographic evaluation of the caudal thoracic vena cava. The jugular vein can be held off and palpated for fullness. If it remains full after it is no longer held off, then preload may be maximized. If it stays or rapidly becomes flat, then additional fluid infusion may be indicated and tolerated. Measuring central venous pressures (CVP) allows quantification of jugular vein distension. In the absence of increased intrathoracic pressure, right heart failure, and obstruction to pulmonary blood flow, an increasing CVP during volume resuscitation supports a volume-responsive condition. Although CVP is not an accurate measure of cardiac output, a lower value (<5 cm H2O) can indicate that additional fluid infusion may be indicated and tolerated. When the CVP measures >8-10 cm H2O in the patient with non-responsive shock, additional fluid infusion is not likely going to be useful and may lead to signs of fluid intolerance (e.g. pulmonary edema, plural effusion). Dynamic changes in the highly compliant caudal thoracic vena cava (VC) diameter during respiration (collapsibility index) identified using M-mode ultrasonography can support a hypovolemic condition. If the difference in the expiratory and inspiratory VC diameter divided by the expiratory VC diameter is 50-100%, then fluid infusion may be indicated and tolerated. Similarly, plethysmography variability index (PVI) is a monitoring variable that identifies pulse variability and measures dynamic changes in perfusion index over respiratory cycles. In mechanically ventilated hypotensive small animals, changes in the PVI > 20 are reported to suggest that hypovolemia is a factor in their hypotension. When volume end-points have been reached, but perfusion end-points have not been reached, causes of non-responsive shock must be investigated for (Table 4). An emergency laboratory data base (packed cell volume and total solids, glucose, venous blood gas, electrolyte levels, lactate level) should be evaluated for evidence of significant anemia, hypoglycemia, severe electrolyte imbalances, severe acid-base alterations and persistent hypoxemia. Evidence of dull heart sounds, a heart murmur, gallop rhythm, or dysrhythmia warrants evaluation of an ECG and cardiac ultrasound. Specific interventions will be based on abnormalities identified. If there has been rapid blood loss, a red blood cell transfusion may be indicated when the PCV<25%. A more insidious drop in the PCV may necessitate a transfusion when the PCV<15-20%. Hypoglycemia is easily remedied with the slow (over 10 minutes) infusion of 500 mg/kg dextrose IV followed by a continuous infusion (1.25-10% dextrose) until the cause has been remedied. Hyperkalemia resulting in cardiac dysrhythmias can be temporarily controlled with slow (over 10 minutes) infusion of 50-100 mg/kg calcium gluconate IV. In addition, 0.2 IU/kg regular insulin IV can be administered followed by 500 mg/kg dextrose IV followed by a continuous infusion (1.25-10% dextrose) until the cause has been remedied. Rarely is 0.1-0.2 mEq/kg sodium bicarbonate infusion. Severe hypokalemia (<2.5 mEq/L) may require slow potassium infusion (over 20-30 minutes) calculated by the following equation: Ideal [K+]-Pt [K+] x vascular volume (L) = mEq K+. Severe hypocalcemia may require calcium gluconate infusion as described above. Severe acidemia and persistent hyperlactatemia may indicate organ ischemia, which may be due to obstruction to blood flow caused by torsion or thromboembolic disease. Opening the conduit to reestablish blood flow is necessary in this situation. Dull heart sounds and evidence of electrical alternans on ECG are supportive of the presence of myocardial tamponade. This may be confirmed by a cardiac ultrasound, and requires pericardiocentesis. A
sustained ventricular tachycardia may require infusion of lidocaine (2-4 mg/kg IV) followed by a continuous infusion (2-4 mg/kg/h). A sustained sinus bradycardia or a-v block (ventricular rate <50 bpm) in the absence of electrolyte imbalances or increased intracranial pressure may be treated with glycopyrrolate, atropine, or temporary pacemaker. A sustained supraventricular tachycardia (>200 bpm) may require careful calcium channel blocker or beta blocker infusion to reduce the heart rate to <180 bpm. If cardiac ultrasound suggests reduced ventricular contractility, then positive inotropic drugs such as dobutamine (dogs: 5-10 mcg/kg/min; cats: 1.5-5 mcg/kg/min), dopamine (3-5 mcg/kg/min), and epinephrine (0.005-1 mcg/kg/min) may be indicated. If hypertension exists, then a Cushing reflex caused by increased intracranial pressure and pheochromocytoma are ruled out or treated accordingly. A Cushing reflex may respond to an infusion of mannitol or hypertonic saline to temporarily reduce intracranial pressure. Alpha blockers such as prazosin may reduce vasoconstriction related to excess catecholamine release caused by a pheochromocytoma. If hypotension exists once the above causes of non-responsive shock have been ruled out, then vasopressors are indicated. Vasopressors such as norepinephrine (1-10 mcg/kg/min), epinephrine, vasopressin (0.03-0.04 units/min), and phenylephrine (1-3 mcg/kg/min) may be used to treat vasodilatory shock. Increased dose dopamine (5-15 mcg/kg/min), can also be used, but may not provide a sustained effect. Dopamine depletes myocardial norepinephrine stores and may become ineffective with prolonged administration. Hemoglobin-based oxygen carriers (HBOC, e.g. Oxyglobinâ&#x201E;˘; 1-3 ml/kg increments up to 15 ml/kg [cat] or 3-5 ml/kg increments up to 30 ml/kg [dog]) can be used to increase arterial blood pressure when fluid challenges fail. Glucocorticoids: At this time, insufficient clinical evidence in companion animals exists to support the administration of high dose glucocorticoids in hypovolemic shock. However, physiologic or low doses of glucocorticoids during resuscitation of the animal in an Addisonian crisis, or vasodilatory (septic) shock not responsive to standard vasopressor infusion can be beneficial. Hydrocortisone is the glucocorticoid of choice in human medicine, and published doses in veterinary medicine are extrapolated from human medicine. Doses suggested for the dog are 0.5-1 mg/kg IV q6h or 0.08 mg/kg/h continuous infusion. Dexamethasone 0.08 mg/kg IV q24 has been used in the fluid-loaded, pressor-dependent cat, but a published dose is not available for dogs. Table 1: Crystalloid and colloid infusion techniques FLUID LARGE VOLUME: Dog Isotonic Replacement Crystalloid 20-30 ml/kg rapid infusion Hydroxyethyl Starch 5-10 ml/kg rapid infusion Table 2: End-point resuscitation goals NORMAL PARAMETERS PERMISSIVE HYPOTENSION MAP 80 - 100 mmHg MAP 60 mmHg HR normal HR < 180 bpm MAP: Mean arterial blood pressure HR: Heart rate
SMALL VOLUME: Dog & Cat 10-15 ml/kg rapid infusion 3-5 ml/kg rapid infusion
Table 3: Infusion technique based on systems affected FLUID
LARGE VOLUME: Dog
SMALL VOLUME: Dog & Cat
END VOLUME
Hypovolemic shock
Hemorrhage Pulmonary disease Cardiac disease Neurological disease Renal disease
Isotonic Replacement Crystalloid
20-30 ml/kg rapid infusion
10-15 ml/kg rapid infusion
60-90 ml/kg
Hydroxyethyl Starch
10-20 ml/kg rapid infusion
3-5 ml/kg rapid infusion
20-30 ml/kg
Table 4: Causes of Non-responsive Shock Inadequate intravascular volume Ongoing fluid losses Severe pain Myocardial depression or failure Cardiac dysrhythmias Myocardial tamponade Electrolyte imbalances Acidemia/alkalemia Hypoglycemia rgan ischemia Hypoxemia Inadequate oxygen carrying ability Glucocorticoid deficiency Decreased venous return (obstruction to blood flow) Excessive peripheral vasodilatation Excessive peripheral vasoconstriction (e.g. pheochromocytoma) ď&#x201A;ŻMAP and/or Tachycardia
Analgesia Fluid Challenge + Rewarming
Anemia
Hypoglycemia
Hyperkalemia ER Database VBG, PCV/TS, Electrolytes, BG, Lactate
Hypocalcemia
Hypercarbia ECG + CC Cardiac US Hypoxemia Vasopressors Metabolic acidosis Corticosteroid
Hyperlactatemia
Suggested Reading Balakrishnan A, Silverstein D. Shock Fluids And Fluid Challenge. In Textbook of Small Animal Critical Care, Silverstein D, Hopper K (eds). Philadelphia: Elsevier, 2014, pp321-327. Rudloff E, Kirby R. Colloid fluid therapy. In Kirkâ&#x20AC;&#x2122;s Current Veterinary Therapy XV. Saunders-Elsevier, St. Louis, MO. 2009; pp8-13 Rudloff E, Kirby R. Fluid resuscitation in the trauma patient. Vet Clin North Amer Small Anim Prac 2008 38(3) 645-652. Burkitt-Creedon, JM. Controversies surrounding critical illness-related corticosteroid insufficiency in animals. J Vet Emerg Crit Care 2015;25:107-112. Reems MM, Aumann M. Central venous pressure: Principles, measurement, and intervention. Compen Contin Educ Pract Vet 2012;34(1) www.vetlearn.com. Chow RS, Dilley P. Central Venous Pressure Monitoring. In Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care, Jamie M. Burkitt-Creedon (Editor), Harold Davis (Editor) Wiley Blackwell, pp145-158. Muir WW. A new way to monitor and individualize your fluid therapy plan. Vet Med 2013 2:76-82. Wehausen C, Kirby R, Rudloff E. Evaluation of the effects of bovine hemoglobin glutamer-200 on systolic arterial blood pressure in hypotensive cats: 44 cases (1997-2008). J Am Vet Med Assoc. 2011 Apr 1;238(7):909-914.