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Emergency Medicine/Critical Care Harold Davis, BA, RVT, VTS (ECC) Veterinary Medical Teaching Hospital University of California, Davis Stabilizing the Trauma Patient Trauma is a wound or injury occurring as a result of an animal's body striking or being struck by an object, from environmental, chemical and thermal insults, or injuries inflicted by other animals. Motor vehicle, animal interactions and trauma of unknown cause comprised 70 to 80% of all injuries in dogs and cats in one study. The most frequent sources of trauma are mechanical forces. These forces produce injuries that can be explained by the physical laws governing acceleration, inertia, momentum, and the absorption and dissipation of energy. Trauma results in disruption and / or impairment of tissues, cellular damage, and organ dysfunction. In addition, mild to severe or even, fatal hemorrhage can occur. Trauma patients may have multisystemic problems, which require rapid and accurate assessment, and treatment. This discussion will address pathophysiology, assessment, management and monitoring of the thoracic, head, abdominal, and musculoskeletal trauma patient. In addition, hypovolemia will be discussed. Primary Survey and Resuscitation When presented with a trauma patient a primary survey is performed. The primary survey is the initial, brief assessment, which addresses the ABCDEs of emergency care ( A) airway, B) breathing, C) circulation D) for dysfunction or disability of the central nervous system, and E) for examination). When a life-threatening problem is identified during the primary survey then resuscitative action should be instituted immediately. Secondary Survey Following the primary survey a secondary survey is performed. The secondary survey is the timely, systematic, and directed evaluation of each body system for injury. Injuries of a lower priority are addressed following initial stabilization. A thorough head to tail physical examination and history are completed. Finally, a comprehensive plan of diagnostics and monitoring is developed and carried out. THORACIC TRAUMA Trauma of the thorax can result in pleural filling defects such as pneumothorax, hemothorax and diaphragmatic hernia. Other problems include rib fractures / flail chest, pulmonary and myocardial contusions. Pathophysiology A simple pneumothorax is caused by the presence of air in the pleural space. The air comes from the outside through the chest wall, from a defect in the lung or both. A tension pneumothorax is caused by air entering the pleural space via a one-way valve flap without the ability to escape. Intrapleural pressure exceeds atmospheric pressure. The accumulation of air permits the separation of the visceral and parietal pleural surfaces. As the separation expands the lung collapses. Hypoxemia ensues because of a ventilation perfusion mismatch. Venous return may decrease owing to the loss of negative pleural pressure. Blood in the pleural space constitutes a hemothorax. Blood comes from several sources such as the lung, intercostal vessels, or systemic arterial vessels. Small amounts of blood do not usually cause detectable signs, while blood loss sufficient to cause hypovolemia (30 - 60 ml/kg) can affect ventilation. Penetrating and / or blunt trauma can cause diaphragmatic hernias. A tear occurs in the diaphragm allowing abdominal contents to enter the thorax. The severity of respiratory distress is dependent on the amount of abdominal organs in the pleural cavity. The space occupied by the organs can restrict lung expansion and reduces ventilation. Rib fractures may cause pain, hemorrhage (owing to laceration or tear of intercostal arteries), and injury to the pulmonary parenchyma. When three or more adjacent ribs are fractured this is termed a "fail chest". These patients display a paradoxical breathing pattern (flail segment collapses in on inspiration and expands out during exhalation). It is thought that the flail chest causes minimal respiratory compromise and that it is the presence of pulmonary contusions that is the major contributor to hypoxemia in these patients. Pulmonary contusions are caused by the transmission of mechanical forces to the thoracic cage resulting in increased tissue pressure and tearing of tissues. Direct laceration may occur from displacement of rib fractures or chest wall compression causing intersitial and alveolar bleeding. Ventilation perfusion mismatch and loss of lung compliance may occur as a result of the pulmonary parenchymal damage. The end result is hypoxemia, increased work of breathing, and with severe lesions, hypercarbia. The heart lies between the left and right thoracic wall. Myocardial contusions result from the compression of the heart, between the ribs and the bruising of the myocardium. The injury can cause alteration in the hearts electrical conduction system leading to arrhythmias, decreased cardiac output and poor oxygen delivery. Patient Assessment First, patency of airway and adequacy of ventilation should be assessed. This is done by visualization, auscultation, and palpation. When looking at the animal, you can determine if the animal is tachypneic or having difficulty breathing. Some animals with respiratory distress may assume a posture with the head and neck extended with abducted elbows. Additional signs include absent chest wall motion, exaggerated ventilatory effort, flaring of the nares, open mouth breathing and paradoxical breathing. Cyanosis may be seen, indicating hypoxemia. Animals with small and large airway problems may have noisy breathing, either stridor / sonorous or wheezes which is suggestive of partial airway obstruction or bronchoconstriction respectively. Patients with absent or diminished breath sounds and a rapid shallow breathing pattern are suggestive of pleural filling defects (Pneumo/hemo thorax and / or diaphragmatic hernia). The chest wall may be palpated to assess chest wall integrity. Crepitus about the body may be due to subcutaneous emphysema, which can be caused by tracheal tears, or chest wall defects. Radiographic imaging can be helpful in making a diagnosis of pleural filling defects, rib fractures and pulmonary parenchymal injury. Contrast agents may be required to diagnose a diaphragmatic hernia. Ultrasound may also be helpful in the diagnosis of diaphragmatic hernia The end result of pulmonary related trauma is hypoxemia. Arterial blood gases and / or pulse oxymetry can aid in the diagnosis of hypoxemia. Hypoxemia is defined as a PaO2 of ? 80 mm Hg or an SPO2 ? 91%. Patient Management Oxygenation supplementation should be provided until it is proven that it is not required. Thoracentesis is performed in patients with signs suggestive of pleural filling defects. If the thoracentesis has to be repeated frequently or if a pleural effusion is present a thoracostomy tube and intermittent or continuous chest drainage may be warranted. If the patient is hypovolemic secondary to a hemothorax, fluid resuscitation will be required. Treatment for diaphragmatic hernia should be as for any patient in respiratory distress. Surgical reduction and repair is the definitive therapy. Some debate exists whether surgical repair should be performed as soon as possible or can be delayed until the patient is stable. Immediate surgery is commonly recommended when the stomach is in the chest. Patients with acute diaphragmatic hernia should be monitored continuously for respiratory compromise and clinical deterioration. Rarely is surgical intervention required for flail chest. Oxygen therapy and pain control are essential. In those cases where the flail chest hinders ventilation mechanical ventilation will be required. Therapy for pulmonary contusions is supportive in nature with the goal of maintaining adequate ventilation and oxygenation. Fluid therapy should be administered to correct perfusion deficits and over hydration should be avoided. Monitoring with central venous pressure measurements and careful and frequent auscultation of the chest may help in tailoring fluid therapy requirements. Mechanical ventilation may be required in some patients with severe pulmonary contusions and respiratory compromise. Ventricular arrhythmias are a sequela of myocardial contusions. Anti-arrhythmics such as lidocaine are administered if the patient is cardiovascularly compromised. In addition, the patient is assessed and treated for extracardiac influences on cardiac conduction disturbances (acidosis, hypovolemia, hypoxemia, hypokalemia and pain). Monitoring Several questions are asked when monitoring the respiratory system. Is the rate and tidal volume adequate; is the breathing effort smooth and easy or labored; is the breathing pattern regular? Can normal breath sounds be ausculted? Abnormal breath sounds could be described as crackles, wheezes, squeaks, muffled and quiet. Is the patient able to meet its ventilation and oxygenation requirements? Arterial blood gases (ABG) are an excellent way to assess ventilation and oxygenation. PaCO2 tell how well the patient is ventilating. PaO2 tells how well the patient is oxygenating. Pulse oximetry, is a non-invasive technique that continuously measures arterial oxygen saturation of the blood. In some instances repeated imaging will be required to assess the status of the thoracic injury. HYPOVOLEMIA Trauma has multisystemic effects, one of which is hypovolemic shock. Hypovolemic shock is a decreased circulating blood volume. Pathophysiology Usually some initiating cause (blood loss, severe dehydration or maldistribution of body fluids) results in a decreased circulating volume. The initiating cause results in a decreased venous return, which leads to a decreased stroke volume, decreased cardiac output and finally a decreased blood pressure and oxygen delivery. In response the body activates the sympathetic nervous system (SNS) causing a release of epinephrine and nor -epinephrine, the end result is an increase in cardiac output. In addition to the activation of the SNS stimulation the body releases rennin /angiotensin and aldosterone as well as vasopressin. These hormonal responses cause increased retention of fluids. Fluids also shift from the interstitium in an effort to increase circulating intravascular volume. The end result is increased cardiac output, increased circulating blood volume and increased tissue perfusion and oxygen delivery. Patient Assessment Does the history or physical findings support evidence of blood loss? Many of the signs that we see suggestive of hypovolemic shock are a result of a compensatory sympathetic reflex. Clinical signs include: tachycardia, pale or grey mucous membranes, prolonged capillary refill, poor pulse quality, cool extremities, and decreased urine production. Patient Management Oxygen therapy is initiated, hemorrhage is controlled and fluid therapy is initiated. Fluid resuscitation improves inadequate tissue perfusion. Options for fluid resuscitation include crystalloids (Lactated Ringers, Normosol R, Plasmalyte 148, and Normal Saline), and Colloids (Plasma, Dextran 70, Hetastarch, and whole blood). Initially, crystalloids are the fluid of choice in the treatment of hypoperfusion. The dose is 80 - 90 ml/kg and 50 - 55 ml/kg in the dog and cat respectively (equivalent to one blood volume). It may be necessary to use 0.5 - 1.5 times the blood volume to resuscitate the patient. 90 % of the crystalloids shift from the intravascular space into the interstitial space in about thirty minutes. Hypertonic saline (7.5% Sodium Chloride Injection USP: Sanofi Animal Health) has been recommended for use in hypovolemic shock therapy in cases where it is difficult to administer large volumes of fluids rapidly enough to resuscitate the patient. Hypertonic saline causes fluid shifts from the intracellular space to the extracellular (including intravascular) space resulting in improved venous return and cardiac output. Hypertonic saline also causes vasodilation and improves tissue perfusion. The recommended dose range is 4 - 6 ml/kg over five minutes. Dextran 70 has been added to hypertonic saline to potentiate and sustain vascular augmentation. Colloids are classified as either synthetic (Dextran 70, Hetastarch or Oxyglobin® or naturally occurring (Plasma, whole blood or packed RBCs). Colloids are better blood volume expanders, 50 - 80% of the infused volume remains in the intravascular space. Colloids should be administered when crystalloids are not improving or maintaining blood volume restoration. Colloids should be administered when the total protein or albumin are decreased below 4.0 g/dl or 1.5 g/dl respectively. Plasma provides albumin, immunoglobulins platelets and clotting factors. Large volumes of plasma may be required to affect total protein or albumin concentrations. The approximate dose of plasma is 10 - 40 mL/kg; however, it should be administered to effect. Dextran and hetastarch may be given as a bolus of 10 - 40 mL/kg to effect. Because the synthetic colloids only replace intravascular volume, crystalloids still must be given to replace interstitial fluid deficits. Crystalloids are given at fifty percent of the dose had crystalloids been used alone. Hemoglobin must be available in sufficient concentrations to insure adequate oxygen content. If hemoglobin decreases from 15 gm/dl to 10 gm/dl, oxygen content is reduced by one third; cardiac output will need to increase in order to maintain adequate 0xygen delivery. In the absence of hemoglobin measurements, hemoglobin can be estimated from the micro-hematocrit. The hemoglobin is usually about one third the hematocrit value. The hematocrit should be maintained around twenty-five percent. Oxygen delivery is limited when the hematocrit decreases below twenty percent. Whole blood and packed red blood cells are administered at 10 - 30 ml/kg and 5 - 15 ml/kg, respectively; again, this will need to be administered to effect. These doses will increase the hematocrit approximately five to fifteen percent. Oxyglobin® solution is a alternative to whole blood or packed red blood cells. Oxyglobin® is a hemoglobin-based oxygen carrying solution. It contains 13 g/dl bovine polymerized hemoglobin in a modified Lactated Ringer's solution. Due to its molecular size it exerts a colloid oncotic pressure effect, which may be beneficial. The manufacturer recommended one time dose range is 10 - 30 ml/kg not to exceed a rate of 10 ml/kg/hr. The patient's condition should be monitored and the fluid given to effect. Administration of hemoglobin (either whole blood, packed RBCs or Oxyglobin®) improves O2 content and ultimately oxygen delivery. Sympathomimetics, such as dopamine and dobutamine are indicated when the patient is unresponsive to vigorous fluid therapy and arterial blood pressure, vasomotor tone, and tissue perfusion have not returned to acceptable levels. These drugs support myocardial contractility and blood pressure with minimal vasoconstriction. If these drugs are used blood pressure monitoring is necessary. Sympathomimetics should not be a substitute for adequate volume restoration. Monitoring Physical exams are repeated as frequently as dictated by the patient's condition. Assessment of the cardiovascular system may begin with the heart rate. The heart rate is a nonspecific parameter; there are several reasons for tachycardia and bradycardia. If arrhythmias are auscultated then an ECG is indicated. The ECG measures electrical activity; it does not measure mechanical activity. Indicators of peripheral perfusion include: mucous membrane color, capillary refill time, urine output and appendage temperature. A full strong pulse indicates a good pulse pressure and stroke volume. Arterial blood pressure is the product of cardiac output and systemic vascular resistance. Normal systolic, diastolic, and mean blood pressure are approximately 100-160, 60-100, 80-120 mm Hg respectively. Central venous pressure (CVP) measures the relative ability of the heart to pump the quantity of blood returned to it. CVP is also an estimate of the relationship between blood volume and blood volume capacity. It can be an indirect indicator of preload. Normal CVP ranges 0-10 cm H2O. CVP measurements require the placement of a jugular catheter, which lies in the anterior vena cava and attachment to a water manometer or transducer. A CVP of < 0 Cm H2O suggest vasodilation or hypovolemia. HEAD TRAUMA Pathophysiology Primary brain trauma is the physical disruption of intracranial structures that occurs immediately at the time of the traumatic event. The injury may be surface mechanical and / or shear injury. Once the injury has occurred nothing can be done to change it. Secondary brain injury is the activation of multiple inflammatory cascades. Activation of inflammatory cascades may result in edema, hemorrhage, increased intracranial pressure (ICP), decreased tissue perfusion, and / or neuronal cell death. ICP is the pressure exerted by the brain, blood and CSF in the cranial vault. An increase in any one volume must be accompanied by a decrease in another so as to minimize any increase in intracranial pressure. This is called the Monro-Kellie doctrine. Cerebral perfusion pressure (CPP) is the principle determinate of cerebral blood flow, brain oxygenation and nutritional support. It is calculated by CPP = MAP- ICP. One of the major contributors to CCP is mean arterial blood pressure (MABP). As MABP rises, cerebral vasoconstriction prevents an increase in ICP. As MABP falls, vasodilation occurs, vasodilation prevents ICP decrease. This is called pressure autoregulation. CPP compromise results in ischemic death of brain tissue Chemical autoregulation refers to the responsiveness of cerebral vasculature to PaCO2; increased PaCO2 causes vasodilation and decreased PaCO2 causes vasoconstriction. Cerebral vasodilation contributes to increased cerebral blood flow and increased ICP. Patient Assessment The physical examination will focus on neurological parameters. The following parameters suggest neurological deficits: decreased levels of consciousness (Obtunded, stuporous and comatose), pupillary light reflex (Pupils that are poor to non-responsive with unilateral or bilateral mydriasis, bilateral miosis, or pupils that are miotic and become mydriatic), abnormal posture (Shiff Sherrington, decerebellate, and decerebrate); and neurologic breathing patterns (Biots, Cheyne stokes, central neurogenic hyperventilation and apneustic), inappropriate response to painful stimuli. If the facility has the capabilities, imaging is beneficial once the patient is stable. Computed tomography is superior to magnetic resonance imaging for examining bone and identifying areas of acute hemorrhage and edema. Radiography rarely provides useful information except when depressed skull fractures are present. Patient Management The patient should be treated for hypovolemia if present, fluid therapy should be conservative but adequate. Osmotic therapy such as mannitol (0.25 - 0.5 g/kg (over 10 - 20 minutes)) should be administered if indicated. Events (increased blood pressure, hypercapnia, and hypoxemia) or drugs (alpha 2-agonist, ketamine, and inhalational anesthetics) that increase intracranial blood flow should be avoided. Events that decrease intracranial outflow (Jugular vein obstruction, coughing, aggressive ventilation, and a head-down position) are avoided. Maintain normal temperature and control seizures. Monitoring The same neurological parameters that are used in the initial assessment are continued in the monitoring phase. The patient is observed for signs suggestive of increasing intracranial pressure. The signs include: deterioration of level of conciseness, change in resting pupil size and loss of pupillary light reflex and the sudden appearance of dilated unresponsive pupils. Intracranial pressure monitoring may be used if available. Other physiological parameters are assessed such as blood pressure, arterial PaO2 or SPO2 and PaCO2 or end-tidal CO2. Electrolytes and osmolality are evaluated with repeated mannitol administration. ABDOMINAL TRAUMA Hemo and uroperitoneum are perhaps the more common intra-abdominal injuries. Bilary tract rupture is rare. Pathophysiology Injuries to the abdomen are primarily penetrating or blunt trauma. Penetrating injuries such as projectiles or stab are more readily visible. The path of the injury is frequently visible and can help localize the possible injured organs. Penetrating injuries my cause bleeding from major vessels or solid organs or perforation of a segment of bowel. Blunt trauma to the abdomen results in compression and shear injuries. Compression injuries occur when the abdomen is crushed between solid objects. Shear injuries occur when there is the rupture of solid organs or vessels in the cavity because of the shearing or tearing forces exerted against their stabilizing ligaments or vessels. Pelvic fractures can cause bladder or urethral injuries. Large hemorrhage into the abdomen can be the major reason for the development of hypovolemic shock. Perforation of the gastrointestinal track can result into the development of peritonitis. Assessment Knowledge of the mechanism of injury is helpful in the assessment of intra-abdominal trauma. Palpation can reveal abdominal tenderness, splinting and or distension. It is helpful to clip the fur over the abdomen in order to visualize abdominal bruising. The abdomen should be observed for distension, contusion, abrasion, penetration, evisceration, impaled objects and / or obvious bleeding. These are all signs suggestive of underlying bleeding. Intra-abdominal hemorrhage should be considered when there is an unexplained reason for hypovolemic shock. Abdominal centesis or diagnostic peritoneal lavage can aid in the diagnosis of intra-abdominal bleeding, peritenontitis, bladder rupture, and abdominal contamination. If this diagnostic tool is to be utilized it should be done following imaging so as not to introduce gas into the abdomen. Analysis of fluid recovered from a diagnostic peritoneal lavage will aid in the diagnosis of uroperitoneum. Serum and lavage fluid, creatinine /potassium levels are compared. If the lavage sample exceeds the serum sample that is diagnostic for uroperitoneum. Imaging can be extremely helpful in diagnosing intra-abdominal trauma. Radiographs with or without contrast are beneficial in diagnosing displaced or ruptured organs, masses, peritoneal effusion, and free gas. Once uroperitoneum is diagnosed, positive contrast studies of the urinary tract are warranted. Excretory urograms will assess the integrity of the kidneys and ureters while positive contrast studies of the urethra and urinary bladder provide more detailed evaluation of the lower urinary tract. Ultrasound, computed tomography and magnetic resonance have all been used to assess abdominal trauma. Patient Management Hemoperitoneum is one of the more common serious complications from blunt trauma to the abdomen. Hemoperitoneum should be considered in any trauma patient that presents in shock without signs of external hemorrhage or thoracic cavity abnormalities. Severe bleeding usually occurs from the spleen or liver although avulsion of the kidney and other organs may cause substantial hemorrhage. As in all hypovolemia cases fluid therapy is the treatment of choice. Fluids should be given in sufficient quantities to support and maintain tissue perfusion but not create a hypertensive state. The fear being that the hypertension could aggravate the abdominal bleeding. Abdominal counter pressure may be used to arrest or control hemorrhage. If this technique is employed care and consideration should be given not to interfere with breathing owing to the increased abdominal pressure on the diaphragm. Abdominal wraps are contraindicated in the diaphragmatic hernia patient; there is the potential that more abdominal organs may be forced into the chest. The decision to go to surgery is difficult. In those cases where free gas is evident on radiographs immediate surgery is necessary. Surgical repair and generous lavage is the treatment of choice when uroperitoneum is diagnosed. Monitoring Because hypovolemia is one of the more common problems encountered with abdominal trauma, those parameters that are monitored during resuscitation should continue. A urinary catheter may be placed to give a better idea of urine production. Abdominal girth should be observed. The patient should be observed for signs suggestive of pain. Depending upon the type of abdominal trauma, the patient may be at risk for the development of a systemic inflammatory response (SIRS). SIRS requires a high index of suspicion and therefore should be a consideration in the monitoring of the patient. CBC, serum chemistry, electrolytes and blood gases are repeated as needed. MUSCULOSKELETAL Pathophysiology The musculoskeletal system is a very large system and prone to many types of trauma related injuries. There are perhaps 5 major injuries that can involve the musculoskeletal system. These include hemorrhage, instability (fractures and dislocations), loss of tissue (avulsion and amputation), simple lacerations, and interruption of blood supply. Assessment Initial examination of the musculoskeletal system entails observation and palpation. Deformity, bleeding, guarding, and pain may be indicators of musculoskeletal injury. Spinal injuries can be causes of neurological deficits. A neurological examination will need to be performed to localize lesions. Care should be exercised so as not to cause further trauma when assessing the patient. Radiographic imaging will provide a definitive diagnosis of skeletal problems. Management The basic premise of musculoskeletal management in the emergency patient comprises the immobilization of the spine or limb to prevent further injury and the appropriate treatment of open wounds. Those patients that are unable to rise following trauma or are displaying opisthotonic postures should be treated as if they are spinal trauma patients. If possible they should be immobilized on a backboard until the status spinal status is known. Where possible, temporary immobilization of the extremity fractures is undertaken to: prevent motion of the bone fragments that could damage muscles, nerves and blood vessels, or cause skin laceration (allowing a closed fracture to become open); control excessive bleeding; and minimize pain. Until definitive care can be provided, a sterile dressing is applied to any open wounds. The wound should remain covered in the hospital environment; this procedure decreases the risk of bacterial contamination and hospital-acquired infection. Further wound treatment is undertaken after patient stabilization. Monitoring The patient is assessed and treated for pain. If an immobilization device is utilized on an extremity the patient's toes should be checked for warmth and swelling. Abnormal smells emanating from bandages or splints are investigated. Soft tissue injuries should be observed for bleeding, swelling, and / or redness. Monitoring the Critically Ill Patient: What Does it All Mean? The hallmark of critical care is monitoring, reevaluation, and assessment. Once you have completed these three steps you must then act on your findings. It is not acceptable to ignore any negative findings in hopes that they will go away. It is also helpful to monitor as many parameters as possible in regards to a particular body system. By monitoring several parameters you will be able to get a better handle on the respective system. A brief overview on the topic of oxygen delivery will be presented. Many of the components of oxygen delivery are routinely monitored in practice. The relationship between oxygen delivery and patient monitoring will be discussed. OXYGEN DELIVERY In critical care we are always concerned that the patient's oxygen delivery is sufficient to sustain life. Oxygen delivery (DO2) represents the amount of oxygen transported to the tissues each minute in millimeters. Oxygen delivery is the product of cardiac output and oxygen content. Oxygen delivery should exceed 600 mL/min/M2. When DO2 is low, an assessment is made of the two determinants of DO2 and therapy is directed at one or both of the determinants. Low DO2 can be defined as oxygen delivery not meeting oxygen demands. There are several factors that contribute to oxygen delivery (Figure 1) 
Figure 1 Determinants of Oxygen delivery. DO2 - Oxygen delivery, CO - Cardiac output, SV - Stroke volume, HR - Heart rate, Hgb - Hemoglobin, PaO2 - Partial pressure of arterial oxygen CARDIOVASCULAR SYSTEM Heart Rate Heart rate is a nonspecific parameter. It is usually measured by auscultation of the heart and palpation of an artery, automatically taken from an ECG or arterial pulse pressure wave. Increase in heart rate (tachycardia) may be caused by hypovolemia (the tachycardia is a compensatory mechanism), fever, excitement, exercise and pain. Tachycardia is generally defined as a heart rate greater than 160 beats per minutes (bpm). Decrease in heart rate (bradycardia) may be caused by high vagal tone, severe electrolyte disturbances and atrioventricular conduction blocks. Bradycardia is generally defined as a heart rate less than 60 bpm. Heart Rhythm When irregularities in heart sounds are heard, the heart rate should be compared to pulse rate and the difference in rates are called pulse deficits. Pulse deficits are indicative of arrhythmias. Hypoxia, myocardial contusions and metabolic or acid base imbalance may cause arrhythmias. Some examples of cardiac arrhythmias include: premature atrial contraction (PAC), atrial fibrillation, premature ventricular contraction (PVC) and ventricular tachycardia. All pulse abnormalities should be confirmed by an electrocardiogram (ECG). Electrocardiographic Monitoring The ECG reflects the electrical activity of the heart. The presence of a normal ECG does not insure effective mechanical activity of the heart. Table 1 Mucous membrane color and its possible significance
When assessing an ECG you should check the following:
It's not necessary that a Veterinary Technician is able to identify all arrhythmias but they should recognize the normals and alert the doctor to the abnormals. Mucous Membrane Color and Capillary Refill Time The normal mucous membrane color is pink (mm color). In diseased states the mm color may be yellow, pale, white, brick red or blue (table 1). Capillary refill time (CRT) is an indication of peripheral perfusion and should not be thought of as an indicator of blood pressure. CRT is the rate at which blood returns to the capillary bed after it has been compressed digitally. To measure CRT lift up the lip and compress the gum with your finger until it blanches out, when you release the pressure the gums should return to their original color within 1 2 Sec. Prolonged CRT is due to vasoconstriction. Vasoconstriction may be caused by hypovolemia, excitement, fear and pain. Central Venous Pressure Central venous pressure (CVP) is a measurement of right atrial pressure. It evaluates three things: 1) The heart's ability to function as a pump; 2) blood volume in relation to volume capacity; and 3) vasomotor tone (indirectly). The normal CVP range is 0 10 Cm H2O. A CVP less than 0 may be due to vasodilation (increased volume capacitance) or hypovolemia. A CVP in a normal range but in the face of signs consistent with vasoconstriction may be due to hypovolemia. A CVP greater than 10 may be due to the heart's inability to function as a pump or fluid over- load, vasoconstriction (decreased volume capacitance), pericardial effusion and positive pressure ventilation. 
Figure 2 Setup for monitoring CVP A catheter placed in the anterior vena cava via the jugular vein is required for measurement of the CVP. To assure proper placement of the catheter, a fluctuation in the fluid meniscus within the manometer synchronous with the heart beat or chest excursions should be seen. A water manometer is placed in the fluid line via a three-way stopcock (Figure 2). The stopcock is turned off toward the patient filling the manometer. The manometer is filled approximately three quarters full. When the manometer is filled the stopcock is turned off toward the IV fluids, this opens the pathway to the patient and the fluid level drops in the manometer. When the fluid stops dropping, note the reading and the zero point is then determined. To determine the zero point a horizontal line is drawn between the manometer and the top of the manubrium. The point where the horizontal line intersects the manometer is the zero point. The difference between the initial reading and the zero point is the CVP measurement. For example the initial reading is 15 Cm H2O, the zero point is 10 Cm H2O the CVP is 5 Cm H2O. CVP measurement is indicated in renal failure, heart failure, shock, and during rapid fluid administration. Arterial Blood Pressure Blood pressure measurement is a valuable monitoring tool when evaluated with other cardiovascular parameters. The trends tend to be more informative than a single value. Blood pressure is a product of cardiac output, vascular capacity and blood volume. These three components are in a careful balance; impairment of one of the components is usually compensated for by the other two so as to maintain adequate blood pressure. The systolic pressure is the maximal pressure obtained with each cardiac ejection. The diastolic pressure is the minimal pressure prior to the next ejection cycle. Mean blood pressure is the average driving pressure, which determines cerebral and coronary perfusion. Mean blood pressure can be estimated by the following formula:
We should become concerned when the systolic blood pressure is less than 80 mmHg or the mean blood pressure is less than 60 mmHg. Some causes for hypotension include vasodilation, hypovolemia, arrhythmias, and anesthetic drugs. 
Figure 3 Ultrasonic doppler There are two methods of blood pressure measurement, direct and indirect. Direct measurement requires the placement of an arterial catheter and the use of a transducer and oscilloscope. This method produces the most accurate results and provides continuous systolic, diastolic, and mean blood pressure measurement. There are two methods of measuring blood pressure indirectly. The ultrasonic doppler (Figure 3) measures systolic blood pressure. A doppler crystal is placed over a peripheral artery, the crystal sends out ultrasound energy into the underlying tissue, the flow of the blood reflects back the ultrasound energy and is picked up by the crystal. The reflected energy is converted to an audible signal. A cuff is placed snugly around a leg. If the cuff is too tight you will get an erroneously low reading, likewise, if the cuff is placed too loose you will get an erroneously high reading. The cuff is inflated until you no longer hear the flow of blood, then you slowly deflate the cuff, the first time you hear the flow of blood the systolic pressure is noted. 
Figure 4 Oscillometric blood pressure unit The Cardell® (Figure 4) blood pressure unit utilizes the oscillometric technique. A cuff is applied to a limb and automatically inflated; the cuff detects oscillations in the underlying artery. As the cuff is gradually deflated oscillations are detected. The first detected pulsation is the systolic pressure; the point of maximum pulsation is the mean blood pressure; and the point were oscillations disappear is the diastolic pressure. PULMONARY SYSTEM Breathing Rate The normal breathing range is 8 - 20 breaths per minute (BPM). The breathing rate alone does not provide you with much information regarding the pulmonary system, therefore, the quality of breathing should be considered as well. Eupnea is a normal ventilatory nature and rate. We will define normal ventilatory nature as a tidal volume of 15 ml/kg (normal tidal volume is 10 - 20 ml/kg). Bradypnea is a slow rate without regard to tidal volume. Tachypnea is a fast rate with out regard to volume. Apnea is the absence of any ventilatory effort. Bradypnea and apnea may be caused by intracranial space occupying lesions, drug induced, hypo or severe hypercapnia and medullary respiratory center dysfunction. Tachypnea may be caused by hypoxia, hypercapnia, hyperthermia, pain and metabolic acidosis. Auscultation Auscultation should be performed in a quiet room. The entire lung field should be ausculted and all abnormal lung sounds should be localized and characterized. Crackles during late expiratory or the early inspiratory phase are indicative of bronchopulmonary disease (pulmonary edema). Expiratory wheezes are due to asthma. Pleural effusion can be characterized by muffled lung sounds. Localized areas of dullness may be caused by atelectasis or lobar consolidation while generalized dullness may be caused by pneumothorax. Mucous Membrane Color Cyanosis may be indicative of severe hypoxia, when it occurs it is usually later in the disease process. For cyanosis to occur, 5 g/dl of un oxygenated hemoglobin must be present. If anemia is present cyanosis may not be seen. Other differentials to consider when cyanosis is seen include: methemoglobinemia and peripheral stagnation of blood flow during shock. In these two instances pulmonary function and PaO2 may be normal. Blood Gas Analysis One of the best ways to assess pulmonary function is through arterial blood gases. Blood gases tell us about the patient's ability to ventilate and oxygenate. Blood gases measure the partial pressure of carbon dioxide (PaCO2) and oxygen (PaO2) in the blood. Blood gas measurements are performed on a blood gas analyzer, this is an expensive piece of equipment to maintain, however, recently a new inexpensive portable pH and blood gas analyzer has been developed. The I-STAT® (Figure 5) blood analyzer may be financially and technically feasible for use in private practice. An alternative to owning an analyzer is to take the blood sample to the nearest human hospital; perhaps arrangements can be made wherein they will run the sample for a minimal fee. 
Figure 5 Point of care lab analyzer. The unit will measure blood gases, electrolytes and other analytes. PaCO2 measures the patient's ability to ventilate. The normal PaCO2 is 40 mmHg with a range of 35 - 45mmHg. A PaCO2 less than 35 mmHg (hypocapnia) is indicative of hyperventilation (excessive elimination of CO2). A PaCO2 less than 20 mmHg may lead to decreased cerebral blood flow leading to cerebral hypoxia. A PaCO2 greater than 45 mmHg (hypercapnia) is indicative of hypoventilation (decreased elimination of CO2). A PaCO2 greater than 60 mmHg may be associated with hypoxemia if the patient is breathing room air. When a PaCO2 reaches this level, ventilator therapy may be required. Hypercapnia may be caused by CNS disorders, pleural filling disorders, abdominal or thoracic restrictive disorders and pulmonary parenchymal disease. PaO2 measures the patient's ability to oxygenate the blood. The normal range is 90 - 100mmHg. A PaO2 less than 60 mmHg is considered hypoxemic and therapy may be started at this point. Some causes for hypoxemia include hypoventilation, ventilation perfusion - mismatch, right to left shunt and diffusion impairment. When the inspired oxygen concentration exceeds 21 percent, expected PaO2 values are different. To determine the expected PaO2, multiply the inspired O2 concentration by five. Thus the expected PaO2 on sixty percent O2 should be at least 300 mm Hg (60x5). The expected PaO2 value represents the oxygen level achievable in the normal healthy lung. Actual PaO2 values that fall below the expected value suggest poor lung function. The PaO2/FIO2 ratio is another index of hypoxemia. A ratio less than 300 indicates a severe defect in gas exchange. A value less than 200 meets the criteria for acute respiratory distress syndrome (given the proper clinical conditions). For example a patient has a PaO2 of 100 mm Hg and it's FIO2 is 40%, it's PaO2/FIO2 ratio is 250 (100/.40) Assuming PaCO2 is reasonably stable, this ratio is a useful assessment parameter in patients with varying PaO2 and FIO2's. Collection of a blood sample for blood gas analysis entails percutaneous puncture of an artery such as the dorsal pedal or femoral artery. The sample is collected in a heparinized coated syringe being careful not to introduce air or applying excessive negative pressure, both of which can affect your PaO2 measurement. Once the sample is collected the artery is held off for a few minutes. Air bubbles are expelled from the syringe and the syringe is corked and placed in a ice water bath. Blood gas samples may stay in an ice water bath for several hours before metabolism alters the pH or blood gas values. Pulse Oximetry Pulse oximetry provides noninvasive and continuous information about the percent oxygen bound to hemoglobin. In essence, oxygen saturation is the ratio of oxy-hemoglobin to deoxy-hemoglobin and oxy-hemoglobin. ASpO2" is commonly used when referring to oxygen saturation readings obtained with a pulse oximeter. 
Figure 6 Measuring Sp O2 in a patient receiving flow-by-oxygen Pulse oximeters (Figure 6) emit red and infrared light that is passed through a body tissue toward a receiving photo detector. A pulsating arterial supply is needed for the pulse oximeter to function properly. Oxygen alters light absorption by the hemoglobin molecule. The degree of change in the light transmission is measured as oxygen saturation. SpO2 and PaO2 are related by the oxy-hemoglobin dissociation curve, one value can be derived from the other as long as the curve is normal. While both pulse oximeter and arterial blood gases (PaO2 specifically) measure the lungs ability to deliver oxygen to the blood the numbers obtained are quite different table 3. Caution should be exercised when interpreting SaO2 values with animals breathing 100% oxygen. Animals with a PaO2 of 500 or 100 would still show a SaO2 from 98 - 99%, which is hardly a significant difference. End Tidal CO2 Capnography is the measurement of ET CO2; this allows the continuous monitoring of exhaled carbon dioxide by analyzing samples obtained directly from the airway (Figure 7). Carbon dioxide readily diffuses across the capillary membrane and quickly equilibrates with alveolar gas. As these gases are exhaled, the CO2 at the end of the breath, or the ET CO2 closely approximates arterial CO2. Normal ET CO2 is approximately 1 - 4 mm Hg less than the PaCO2. Factors affecting measurements include gas leaks, sensor obstruction, and taking readings during the early part of exhalation. 
Figure 7 Example of a capnograph CENTRAL NERVOUS SYSTEM Like all other systems it is important to establish a baseline when evaluating a body system and then monitor the trends. This is especially true with the central nervous system (CNS), subtle changes can take place that require astute monitoring abilities. Therefore, the patient should be monitored frequently and the results recorded. Any deterioration in the monitored parameters should be brought to the attention of the clinician. Consciousness Level Consciousness may be categorized into four levels. Normal, obtunded, stuporous and coma. An obtunded patient is one who has mild to moderate reduction in alertness and often appears drowsy, but is easily aroused. Stupor is a condition characterized by a deep sleep that is only responsive to vigorous or painful stimuli, once the stimulus is removed the patient returns to its sleep like state. The comatose patent is totally unresponsive even to painful stimuli. It is a poor sign when a patient moves from a higher level of consciousness to a lower level. Posture When evaluating posture the concern is for the presence or absence of abnormal posture associated with opisthotonos. Opisthotonos is a form of spasm in which the head is bent backwards and the body bowed forward. The three types of abnormal posture include Schiff-Sherrington, decerebellate rigidity and decerebrate rigidity (Figure 8) (each posture has a opisthotonic component). Schiff-Sherrington is due to a severe spinal cord injury. With Schiff-Sherrington, the patient's front limbs are in extensor rigidity and the rear limbs are relaxed. The patient has a normal level of consciousness. Prognosis is poor. Decerebellate posture occurs with severe cerebellar injury. The patient's front limbs are in extensor rigidity while the rear limbs are flexed. The patient has altered mentation. The prognosis is fair for this posture. Decerebrate posture is due to a severe brain stem injury; extensor rigidity is present in both front and rear limbs. The patient is unconscious. The prognosis is poor for this posture. Should any of these postures develop it should be brought to the attention of the Veterinarian. 
Figure 8 Patient with decerebrate posture Pupil Size Normally pupils should be equal in size and have a direct and consensual response to light. If the pupils are fixed in a midpoint position and unresponsive to light a severe midbrain lesion is suspected and the prognosis should be considered guarded. If there are changes in the pupils especially the fixed midpoints a-reflexic, notify the clinician. Breathing Patterns There are several breathing patterns that are a result of CNS lesions. They are as follows:
Urinary output is an excellent reflection of tissue perfusion. If the kidneys are producing urine then the other organs are probably being perfused. The normal urinary output is 1 - 2 ml/kg/hr. Ideally its important to quantitate the urine output. There are several techniques for urinary collection some examples include: Placing a urinary catheter and using a closed collection system, walking your patient and collecting the urine in a bowl, weighing a disposable diaper and placing it underneath the penis or vulva in a recumbent patient obtaining the difference between the wet weight and dry weight, weighing the litter pan pre and post urination and again obtaining the difference for urine output. 
Figure 9 weighing a patient to help assess fluid balance In addition to quantitation of urine, it is also helpful to quantitate defecation and emesis; this can provide you with a better picture of your total fluid balance. Weight (Figure 9) gains and losses should be monitored on a daily basis if not more frequently. Acute changes in weight are usually a result of fluid changes and not muscle mass. The fluid losses should be compared to fluid intake, they should just about balance out. Any big discrepancy in the "ins and outs" should be brought to the attention of the clinician. BODY TEMPERATURE Core Temperature Placing a deep rectal or esophageal thermometer may monitor core temperature. When monitoring the temperature early recognition of hypo or hyperthermia will result as well as trends in the patients status. The normal temperature for a dog or cat is 101 102.5oF (38.3 - 39.2o C). In the neonate the normal body temperature is 7oF above the environmental temperature during the first week of life. By the second week they can maintain their temperature from 98 100oF (36.6 - 37.7o C). By the forth week their thermal regulation is mature. The causes for hypothermia (Temp < 101 (38.3o C)) include prolonged exposure to a cold environment and peripheral vasoconstriction, causing shunting of blood from the peripheral tissues and GI tract in response to decreased perfusion. The causes for hyperthermia include a hot environment with poor ventilation, a response to infection or inflammation, and thermoregulatory dysfunction. LABORATORY ASSESSMENT Hematocrit and Total Solids Hematocrit (Hct) and total solids (TS) can be used to gauge fluid therapy estimate hemoglobin concentration and, to a certain degree, assess blood loss. The two tests should be interpreted together to minimize errors in interpretation. Increase in both Hct and TS indicate dehydration, decrease in both Hct and TS is suggestive of recent blood loss or clear fluid administration. Increase in TS and normal Hct may indicate anemia with dehydration. Both normal Hct and TS may be normal in peracute blood loss. TS may decrease with reduced albumin levels; albumin is a contributor to oncotic pressure. Blood Glucose Glucose provides an energy source for cells. Hypoglycemia should be considered in patients that are at risk for sepsis; or are hypothermic, seizuring, or exhibiting altered mentation. Marked hyperglycemia can be associated with coma. Electrolytes Electrolytes play a major role in the maintenance of inter-compartmental water balance and cell function. Baseline electrolytes should be obtained and monitoring continued as therapy progresses. Fluid therapy can alter various serum electrolyte concentrations, and may require adjustment of the electrolyte composition in the fluids being administered. Commonly measured electrolytes include serum potassium, sodium, chloride, magnesium and ionized Calcium. Colloid Oncotic Pressure Colloid oncotic pressure (COP) can be measured and used to guide fluid therapy. COP is a force created by large plasma proteins that do not move freely across capillaries. The presence of colloids in the vascular space has the effect of pulling water from the interstitium into the vascular space. The goal is to maintain a COP greater than 15 mm Hg. Lactate When perfusion decreases and oxygen delivery is reduced the body shifts from aerobic to anaerobic metabolism resulting in lactate formation. Elevated blood lactate (lactate > 2 mM/L) has been proposed as an indicator of inadequate tissue oxygenation. Although elevated blood lactate levels often signify generalized tissue hypoxia, a normal value does not rule out regional lactate production. Summary As stated earlier it is important to monitor the trends. To help you keep track of the trends you should use some type of charting system. It need not be an elaborate system but one that will allow you to see all the parameters measured. A critical care patient checklist has been included in these notes to serve as a reminder as to your nursing care considerations when caring for the critically ill patient.
Action Stat: Management of the Emergency Patient PRIMARY SURVEY The primary survey includes the rapid assessment of the patient and the treatment of life-threatening problems as they are identified. The use of the simple mnemonic "ABCDE's of emergency care" (figure 1) helps the technician to remain focused with the major priorities. The ABCDE's of emergency care provide a systematic approach to evaluating or assessing the emergent or critically ill patient.
The primary survey does not require a lot of medical equipment; it does require your ability to use your senses (look, listen, feel, and smell). The primary survey begins with assessing the airway patency, if the airway is patent then the patient's ability and quality of breathing is assessed, if the airway is not patent, it must be cleared and/or the patient intubated, before moving on to breathing. If the patient is not spontaneously breathing then artifical ventilation will need to be instituted. The assessment is continued on to the next body system unless a life-threatening problem is identified. If one is identified, it must be treated before proceeding. Once the primary survey is complete a secondary survey is undertaken. The secondary survey is a complete head to toe physical examination, at this time it may be appropriate to obtain a patient history. PATHOPHYSIOLOGY OF PNEUMOTHORAX Air enters the pleural space causing collapse of the affected lung; subsequent ventilation-perfusion (V/Q) mismatch resulting in hypoxemia. Alteration of pleural pressure gradient impairs thoracic pump and venous return.
PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK Usually some initiating cause (blood loss, severe dehydration or mal-distribution of body fluids) results in a decreased circulating volume. The hypovolemia results in a decreased venous return, which leads to a decreased stroke volume, decreased cardiac output and finally a decreased blood pressure and oxygen delivery. In response, the body activates the sympathetic nervous system (SNS) causing a release of epinephrine and nor -epinephrine, the end result is an increase in cardiac output. In addition to the activation of the SNS stimulation the body releases rennin /angiotensin and aldosterone as well as vasopressin. These hormonal responses cause increased retention of fluids. Fluids also shift from the interstitium in an effort to increase circulating intravascular volume. The end result is increased cardiac output, increased circulating blood volume and increased tissue perfusion and oxygen delivery.
PATHOPHYSIOLOGY FLUTD Urolith (struvite and calcium oxalate) plug can cause urethral obstruction, usually at or near urethral orifice. Urine will backup into the kidneys. This will result in nephron damage. Post-renal uremia and hyperkalemia (due to decreased elimination) may develop.
SUGGESTED MECHANISM OF ARRHYTHMIAS IN GDV - Myocardial ischemia associated with hypotension and caudal vena cava compression - Autonomic imbalance - Fluid, electrolyte, and acid-base imbalances - Myocardial Depressant Factor (MDF) release from the pancreas
PATHOPHYSIOLOGY OF TRAUMATIC BRAIN INJURY Primary brain trauma is the physical disruption of intracranial structures that occurs immediately at the time of the traumatic event. The injury may be surface mechanical and / or shear injury. Once the injury has occurred nothing can be done to change it. The goal is to minimize or prevent secondary brain Injury. Secondary brain injury is the activation of multiple inflammatory cascades. Activation of inflammatory cascades may result in edema, hemorrhage, increased intracranial pressure (ICP), decreased tissue perfusion, and / or neuronal cell death. ICP is the pressure exerted by the brain, blood and CSF in the cranial vault. An increase in any one volume must be accompanied by a decrease in another so as to minimize any increase in intracranial pressure. This is called the Monro-Kellie doctrine. Cerebral perfusion pressure (CPP) is the principle determinate of cerebral blood flow, brain oxygenation and nutritional support. It is calculated by CPP = MAP- ICP. One of the major contributors to CCP is mean arterial blood pressure (MABP). As MABP rises, cerebral vasoconstriction normally prevents an increase in ICP. As MABP falls, vasodilation occurs, vasodilation prevents ICP decrease. This is called pressure autoregulation. Chemical autoregulation refers to the responsiveness of cerebral vasculature to PaCO2; increased PaCO2 causes vasodilation and decreased PaCO2 causes vasoconstriction. Cerebral vasodilation contributes to increased cerebral blood flow and increased ICP. The bottom line, CPP COMPROMISE RESULTS IN ISCHEMIC DEATH OF BRAIN TISSUE.
Critical Care Essentials INTRODUCTION Caring for the critically ill patient can be a challenging endeavor. Clinical expertise is developed overtime and requires the integration of critical care knowledge, clinical skills and caring practices. There are essential, knowledge, skills and abilities that the critical care veterinary technician (CCVT) needs in order to provide safe and competent care to the critically ill patient. It is hoped that the CCVT will build on the essential concepts. In human nursing nurses utilize the nursing process to guide delivery of patient care. The nursing process is a method of making clinical decisions or a way of thinking and acting to a clinical event of concern to the nurse, or in our case the veterinary technician. The nursing process provides an organized, systematic approach to solving clinical problems. Traditionally, the nursing process comprised four phases or components: assessment, planning, implementation, and evaluation. The nursing process is an excellent tool for the novice critical care veterinary technician; it provides the foundation on which to build upon. This discussion focuses on the "essentials" needed to provide nursing care to the critically ill patient and will use some aspects of the nursing process as its framework. CRITICAL CARE ESSENTIALS: THE PREREQUISITES The veterinary technician must have a sufficient knowledge and skill base and the ability to think critically. The knowledge base must encompass basic concepts of anatomy and physiology as well as a basic understanding of common disease processes, diagnostic, and therapeutic procedures. Technicians should also be familiar with potential complications or risk factors associated with these diseases, and procedures. PATIENT ASSESSMENT Assessment of the critically ill patient is an essential competency for the CCVT. Assessment is the data collection and analysis. The basic categories of techniques used in the assessment include patient history, physical examination /observation and measurement. Data may come from a variety of sources. Owners provide a history; members of the health care team share information concerning the patient; the technician or veterinarian performs a physical examination; review of previous medical history and laboratory data for pertinent information; and collection of physiologic parameters (blood pressure, ECG, central venous pressure etc.). Patient History Patient rounds are an excellent forum for communication. Information that should be conveyed during rounds includes: why is the patient in ICU? What are the major problems? What diagnostics were completed during the shift, including laboratory analysis? Note abnormal values and / or changes in trends; what were the highlights of events during the shift - any problems to note; what suggestions or special advice do you have for the new shift? Physical Examination The technician should become skilled at performing a complete physical examinations; it defines the patient's responses to the disease process. The physical exam helps establish a baseline for comparison in evaluating ongoing nursing or medical interventions. At minimum, a temperature, pulse, and respiration should be checked; in addition mentation should be noted, chest auscultated and the bladder palpated. The patient's hydration status should be determined. Of all the body systems, the pulmonary, cardiovascular, and neurologic are of major importance when performing the physical examination. To complete the assessment all catheters, bandages, wound dressings and drainage systems should be checked. Pulmonary System Visually assess ventilation rate, effort and pattern. Does the patient have exaggerated ventilatory effort or minimal or absent chest wall motion? In addition to an increased rate and effort, signs of respiratory distress include open mouth breathing, extended head and neck, abducted elbows, restlessness and unwillingness to lie down. Note whether or not there are audible airway/breath sounds. Diminished or absent breath sounds are suggestive of pleural filling defects such as pleural effusion or pneumothorax. Can you define the abnormal airway/breath sounds (stridor, stertor, crackles or wheezes)? What is the mucous membrane color? Cyanosis is a late and unreliable sign in determining hypoxia. One third of the hemoglobin must be unoxygenated for cyanosis to be evident. In the case of an anemic patient cyanosis may never be seen. Cardiovascular System Assessment of the circulatory system includes the evaluation of mucous membrane color, capillary refill time, extremity temperature, urine production and pulse quality and rate. The heart should be auscultated for rate, rhythm and murmurs. The pulse should be palpated while listening to the heart, there should be a pulse beat for every heart beat ausculted. If there is not a pulse beat fro every heart beat this is termed a pulse deficit. Signs suggestive of cardiovascular compromise include: tachycardia, pale or grey mucous membranes, prolonged capillary refill, poor pulse quality, cool extremities, and decreased urine production. Neurological System Neurological assessment should include evaluation of the level of consciousness, pupillary light reflex, breathing patterns, posture, and response to pain (superficial and/or deep). Signs of neurological deficits include altered levels of consciousness (normal to comatose, or somewhere in between). Progressive constriction, dilation, anisocoria with diminished pupillary light reflex in the absence of ocular trauma is indicative of neurological deterioration. Irregular breathing patterns such as cyclic hyperventilation or cyclic hypoventilation and apnea are also suggestive of neurological problems. It is important to differentiate between decerebrate and decerebellate rigidity. Both are characterized by extensor rigidity in all limbs and opisthotonos. However, in decerebellate rigidity the hind limbs may be flexed or extended. Schiff-Sherrington consists of extensor rigidity of the forelimbs and flaccid hind limbs. It is a poor prognostic sign when a patient doesn't perceive pain. Pricking or pinching the skin tests superficial pain. Applying noxious stimuli to the toes or joint tests deep pain. In both cases the patient should show some visible discomfort. A drowsy or comatose patient and the "Cushing triad" (arterial hypertension, bradycardia, and respiratory irregularities) is suggestive of increased intercranial pressure. Following the nursing assessment and a review of the doctor's orders, plans should be formulated for the nursing care of the patient. ESSENTIAL BASIC CRITICAL CARE SKILLS The CCVT must possess a variety of skills. The Academy of Veterinary Emergency and Critical care Technicians has established a skills list (www.avecct.org) that potential candidates must master prior to taking the exam. The following are just a few of the essential skills or abilities that a CCVT must have. Artifical Airway Management The CCVT should be well versed in the management of an artificial airway (endotracheal tube or tracheostomy tube). At times it may be necessary to gain immediate control of the airway. Endotracheal intubation is the most rapid, atraumatic way to assure a patent airway. The technician must have the technical ability to intubate the patient. Emergency tracheostomy is indicated for partial or complete upper airway obstruction that leads to clinical hypoventilation or severe distress and the patient cannot be intubated. The Technician's role is to gathers the needed supplies (Various sizes tracheostomy tubes, surgical kit, sterile drapes and gloves, and positioning aids) and prepares the patient for surgery. If the patient will have a long term artifical airway it will become the responsibility of the CCVT to maintain the airway. The principles of artificial airway management entail airway humidification, tracheal suctioning, coupage, tracheostomy site care or endotracheal tube care (deflation and repositioning q 4hrs and changing q 48hrs.), and oral care (suctioning the mouth and pharynx, wiping the teeth, gums, and tongue with chlorhexidine mouth wash q 4 hrs). Oxygen Therapy Oxygen therapy can be life saving in almost all cases of respiratory distress caused by hypoxemia. There are many ways to administer oxygen; they all have advantages and disadvantages. Face mask are readily available and easy to use. Masks are only good for short-term use. High-inspired oxygen concentrations can be obtained if a properly fitted face mask is used. Unfortunately, patients often fight the face mask (unless obtunded) thereby increasing oxygen consumption and canceling the effects of the oxygen therapy. An alternative to the face mask is the oxygen bag (or hood). A clear plastic bag is placed over the head of a patient and a hose from an oxygen source is placed near the animal's nose. The bag remains open along the animal's neck to allow the gas to escape. A flow rate of five to eight liters per minute is used. It has been reported that animals tolerate this bag/hood method when they resist the oxygen mask. Oxygen cages are well tolerated by patients. An oxygen cage should have the following features: it must have a system for eliminating carbon dioxide; deliver a known amount of oxygen in a concentration beneficial to the patient (40 - 50%); and a mechanism for controlling temperature (70?F) and humidity (50%). The disadvantages to this system are, it's expensive to operate, the technician has minimal access to the patient and it is difficult to accommodate large patients. Nasal oxygen is an excellent way to provide oxygen therapy. The advantage is, it does not require an expensive O2 cage, you can use supplies found in your clinic, you have direct access to your patients at all times, and it is well tolerated by your patients. Venous Access Intravenous access can literally be the difference between life and death in the emergent or critically ill patient. Once a catheter is in place it may be used to administer fluids and/or medications; provide nutritional support; monitor central venous; or collect blood samples. CCVT should be capable of selecting the proper vessel, placement of different catheter types, utilizing various insertion techniques, and maintaining the catheter. Selection of a vein depends on several factors such as the skill of the operator placing the catheter, available veins, therapeutic goals, and the animal's problem or disease. Any vessel that is visible should be considered a candidate for percutaneous catheterization. Options for venous catheterization include the cephalic, medial and lateral saphenous, femoral, jugular, aural, and abdominal veins. In addition to the commonly used over-the-needle-catheter the technician must be able to place other types of catheters. Catheters passed through the needle are called through-the-needle or inside-the-needle catheters. Through the needle catheters are usually longer than over-the-needle catheters (8" to 12") and are used primarily in the jugular vein. These catheters come in a variety of lengths and diameters. A plastic sleeve to prevent contamination protects the catheters. Multi-lumen catheters are available in both the over-the-needle and through-the-needle style. Multi-lumen catheters have two to three separate lumens in one catheter. Multi-lumen catheters allow simultaneous infusions at one catheter site. Though one catheter is placed, the multi-lumen catheter provides the same functions as two to three separately introduced single-lumen catheters. Catheter placement is usually completed percutaneously with a guide wire or peel-away sheath technique. Multi-lumen catheters are more expensive than the commonly used IV catheters. Catheter maintenance entails catheter site inspection (looking for signs of phlebitis, thrombosis, infection) and / or fluid infiltration), cleansing of the site and re-bandaging. Constant Rate Infusions (CRI) Many analgesics and cardiac or vasoactive drugs are administered as constant rate infusions via syringe pump or fluid infusion pump. With regard to analgesics, the main advantage of a CRI is that it avoids peaks and valleys which are typically seen with opioid bolus dosing. In addition, a lower dose of the drug may be administered over time. Drugs that can be administered as a CRI include lidocaine, morphine, fentanyl and ketamine. Immediately prior to starting a CRI, a loading dose is given. Cardiac and vasoactive drugs have a rapid onset of action and a short elimination half-life and must be administered as a CRI to maintain constant serum concentrations. Cardiac or vasoactive drugs that are administered as a CRI include lidocaine, dopamine, and dobutamine. The CCVT must be able to set up, administer, and monitor the effects of the CRI. There are a few simple formulas that a technician can use to calculate CRIs. Many drugs use a microgram (mcg)/kg/min dosing scheme. 1000 mcg is equal to 1 mg. Formula 1: Drug dosage (mcg/kg/min) x BW (kg) = # mg to add to a solution for a total volume of 250 ml. The CRI is given at a rate of 15 ml/hr. The final volume and concentration remain constant. Formula 2: The following formula solves for the number of mg drug (M) to add to a base solution. M = (D) (W) (V) / (R) (16.67) or The following formula solves for the rate (R) of delivery in ml/hr. R = (D) (W) (V) / (M) (16.67) D = dosage of drug in mcg per kg per min W = body weight in kg V = volume in ml of base solution 16.67 = conversion factor ESSENTIAL BASIC CRITICAL CARE NURSING SKILLS IV Catheter Care IV catheter care should be performed every 48 hours or on an as needed basis. The catheter dressing should be removed and the site inspected. You should look for signs of phlebitis, infection, and or thrombosis. Signs of phlebitis may include erythema, swelling, tenderness upon palpation, and an apparent increase in skin temperature over the vein. The signs of infection are phlebitis and a purulent discharge. Signs of thrombosis include a vein that stands up without being held off and a thick cord like feeling to the vein. When signs of phlebitis or thrombosis are apparent, the catheter should be removed and a new one placed at a different site. While flushing the catheter with heparinized saline, the insertion site should be observed for leaking of fluid at the insertion site and pain upon injection. If either one is observed, the catheter should be removed and replaced with a new one. If any portion of the catheter is exposed, it should be noted. If the catheter site looks good then the site should be cleaned with an iodophor or chlorhexidine solution. When the catheter site is dry, cover the insertion site with a sterile 2x2 gauze pad. Then re-bandage the catheter. Traditionally it has been recommended not to leave a catheter in place any longer than 72 hours. These recommendations come from human medicine. It has been shown that the likelihood of complications increases the longer catheters are left in place. It has been our experience that as long as routine catheter care is performed, and the catheter removed when problems are first noticed, one can often exceed the 72 hour rule. A study looking at peripheral and jugular venous catheter contamination in dogs and cats supports our experiences. IV catheters should be observed several times a day. If the catheter bandage is found to be wet, then the reason should be identified and the bandage should be changed. Swelling distal to the catheter is usually indicative of a tight bandage. Swelling proximal to the catheter may be due to infiltration. Urinary Catheter Care Urinary catheter care is performed every 8 hours. It entails cleaning the prepuce or vulva and its surrounding area with a mild soap and water rinse. The sheath or vestibule is then flushed with a dilute Betadine (weak tea colored) or 0.05% chlorhexidine solution. The urinary catheter itself should be kept clean especially in the female patient where the vulva is in close proximity to the rectum. The urinary catheter should be attached to a collection system. By maintaining a closed collection system you decrease the chance of a urinary tract infection (UTI). Do not disconnect the urinary catheter from the collection system. Drain the system every 2 4 hours rather than hourly. Urinary collection bags may be obtained commercially or you can use an empty sterile IV bag. The addition of 3% Hydrogen peroxide to the urinary collection system has been shown to decrease the incidence of UTI. Five to ten milliliters of hydrogen peroxide is added to the urinary collection system. Chest Drain / Gastrostomy Tube Care The procedure for chest drain and gastrostomy tube care is much like IV catheter care. The bandage is removed and the insertion site is inspected every 24 hours. The site is cleaned and re-bandaged. Nutritional Support The nursing goal is to ensure that the patient is meeting its energy requirements. There are serious negative consequences of acute malnutrition including: decreased immune response, loss of function of tissues and organs and delayed wound healing. A patient's history may be helpful in determining if nutritional support is needed. If it has been three or more days since the patient ate, nutritional support may be indicated. The physical exam might reveal acute loss of lean body mass, fat, muscle wasting, or edema. Hypoalbuminemia and lymphopenia may indicate poor nutritional status. Once it is decided to initiate nutritional support the technician will need to calculate the patient's energy requirements. Most hospitalized veterinary patients can be fed at their calculated resting energy requirement (RER), realizing their actual energy requirements may change over the course of the disease process and recovery. RER can be calculated using either one of the following formulas. The allometric formula (RER (in kcal/day) = 70(BWkg0.75)) is used in dogs and cats of all weights or the linear formula (RER (in kcal/day) = (30 x BW kg)+70) may be used in patients that weigh at least 2 kg. Once the daily caloric requirement (kcal/day) is determined and the diet has been selected, the volume of food to feed is calculated. Divide the daily caloric requirement by the caloric density (kcal/can, kcal/ml etc), to determine the total daily volume of diet to feed. SUMMARY The purpose of this discussion was to provide the essential foundation for the nursing care of critically-ill patients. This was by no means an exhaustive discussion but an overview from which to build. | ||||||||||||||||
