NMBAs and Emergencies Recovery Phase PDF

NMBAs and Emergencies: Recovery Phase: 60% of anaesthetic deaths occur during the recovery phase The ability of the veterinary team to care for our patients effectively relies on prompt and accurate identification of changes to clinical parameters. One challenge is that the recovery phase is typi...

NMBAs and Emergencies: Recovery Phase: 60% of anaesthetic deaths occur during the recovery phase The ability of the veterinary team to care for our patients effectively relies on prompt and accurate identification of changes to clinical parameters. One challenge is that the recovery phase is typically busy with multiple aspects of patient care to monitor. Elements of recovery monitoring include: extubation, wound care, recording medication administration and observations, oxygen supplementation, medication administration, monitoring patients, requesting ongoing diagnostic tests, and balancing demands of other roles and patients. The ability to relate anatomy and physiology knowledge to pathophysiology of shock can help us to understand the clinical signs that may be observable in our patients Reasons behind shock: - Cells in the bloodstream are starved due to lack of oxygen returning to the heart. - Distributive shock, where there is inflammation around the cells preventing oxygen from getting to the cells, meaning that it remains in the bloodstream, which therefore leads to the blood returning to the heart has a higher concentration of oxygen. - Mixed venous oxygen (MVO2)- when blood from the superior and inferior vena cave (brings blood from part of body) meets in the right atrium they mix. Each vena cava might have different mmHg causing them to mix and create an average. - Cells are not receiving enough oxygen used for energy (aerobic metabolism), and anaerobic metabolism is happening instead due to low oxygen. This is when energy is made without oxygen. Not as efficient and therefore, can't reach the energy needs of the cells. - A by-product of the anaerobic metabolism of lactic acid, so when cells are starved of oxygen, there is an increase in this. Causing lower pH level, causing side effects such as heavy breathing in order to expel off CO2 to get rid of acid accumulating. - If the body continues to not receive enough oxygen then it could lead to irreversible damage (liver, kidneys & lungs) Tachycardia: Reasons for tachycardia include inadequate analgesia, hypovolaemia, electrolyte disturbances, hypoxia, anaemia and atrial or ventricular function. It can be very challenging for the veterinary surgeon to interpret one clinical sign in isolation when making an assessment of a patient's progress. Good nursing care involves a wide overview of multiple parameters so that clinical signs can be considered together to create an accurate picture of a patient's status. Trends in parameters identified by serial assessments are crucial to this. Physiology recap: The sinoatrial node is located in the wall of the right atrium and is the pacemaker which initiates each heartbeat. The heart rate, which must be able to vary in order to respond to physiological changes, is controlled by nerves of the autonomic nervous system (ANS) that act on the specialised tissue of the heart. The sympathetic branch of the ANS acts to increase the heart rate whilst the parasympathetic branch acts to decrease the heart rate. A diagram of a human heart Description automatically generated Stroke Volume: affects the delivery of circulation to the tissues Cardiac output = heart rate x stroke volume Cardiac output = Volume of bloods that pumps through the circulatory system in one minute Stroke volume = Volume of blood that is pumped by the left ventricle in one contraction Shock: Working with the definition of shock as the inability to perfuse organs and tissues effectively, and based on the physiology briefly outlined, we can predict the response of the cardiovascular system to the changes that occur in hypovolaemic shock. Responses to shock are predictable in the canine patient but less predictable in the feline patient. In early shock, the body aims to compensate for reduction in perfusion by causing vasoconstriction to support blood pressure and increase cardiac contractility and heart rate. The effects of anaesthetic drugs, however, may make it more difficult to increase heart rate as many have a depressant effect on the cardiovascular system.  Cellular hypoxia results in anaerobic metabolism which produces less ATP than aerobic metabolism and increases waste in the form of hydrogen and lactate ions. These can accumulate in the circulation and eventually cause problems with cardiac rhythm and contractility.  Myocardial oxygen supply is also directly decreased in hypoxaemia at the same time as an increased demand.  Hypercapnia will occur in the event of respiratory depression and circulatory failure returning less CO~2~ to the lungs for excretion.  It will also cause direct depression of cardiac muscle and the reflex stimulation of the sympathetic nervous system to increase myocardial work.  **The end result of untreated shock is an irreversible situation where the circulatory system is exhausted.** Drugs used to treat shock in emergencies are targeted at supporting early compensatory mechanisms and/or reversing the deleterious effects of physiological changes in the later stages of shock. Drugs acting to support cardiac output can be termed as inotropes and chronotropes. Inotropes= Positive ones act to increase the strength of cardiac contraction and increase the stroke volume. Negative ones act to decrease the strength of cardiac contraction and increase the stroke volume. Chronotropes= Positive ones act to increase the heart rate, whilst negative ones act to decrease the heart rate. Fluid balance and shock: In shock, catecholamines are the neurotransmitters of the sympathetic nervous system that mediate vasoconstriction via action on alpha receptors. Simultaneously, the release of renin from the kidney initiates the Renin-Angiotensin-Aldosterone System (RAAS) cascade, the downstream effects of this system being the retention of fluid volume and elevation of blood pressure via the effect of aldosterone acting on the collecting ducts of the nephron.  A related mechanism is the insertion of aquaporin channels into the membrane of cells within the distal convoluted tubule and collecting ducts of the nephron. This is mediated by ADH which is released from the posterior pituitary gland in response to a rise in plasma osmolality. Shock and fluids: Clinical signs associated with shock include slow jugular refill/collapsed peripheral veins, depressed level of consciousness, muscle weakness, hyperdynamic central pulse present in early compensatory stage, tachycardia, tachypnoea, pale MM, CRT more than 2 seconds however CRT may be less than two seconds in early compensatory stage, hypothermia/cold extremities. **Pathophysiology of Shock** Osmoreceptors detect alterations in blood volume and pressure, stimulating the hypothalamus to initiate the release of hormones such as anti-diuretic hormone (ADH), from the pituitary gland, and cortisol, from the adrenal cortex via CRH release/ACTH from the pituitary.  Angiotensin and aldosterone are also produced following renin release in the kidneys. The result of these hormones involves water and salt retention to maintain blood pressure and ensure a continued supply of oxygen and energy.  As well as the endocrine system, changes in the blood volume will also stimulate the nervous system. Initiation of the sympathetic nervous system results in increased heart rate and peripheral vasoconstriction mediated by adrenaline, helping to maintain blood flow to the vital organs such as the brain, heart and lungs.  There are three types of shock - **hypovolaemic**, **cardiogenic** and **distributive**.   **Hypovolaemic Shock ** This is commonly seen in veterinary practice and occurs where there is an absolute fluid loss from the body.  Causes of hypovolaemic shock include:  - Haemorrhage following surgery or trauma - Plasma loss from burns - Third space losses, with fluid accumulation within the uterus (pyometra) or abdomen (peritonitis) - Fluid depletion from severe dehydration **Cardiogenic Shock** Cardiogenic shock occurs primarily due to cardiac insufficiency; *cardio* = heart, *genic* = orginates. The volume within the circulation remains adequate but the heart is unable to pump the fluid around the body effectively.  Causes of cardiogenic shock include:  - Cardiomyopathy (*seen in the radiograph*) - Valvular abnormalities, such as ruptured chorda tendinae - Arrhythmias, such as atrial fibrillation - Obstructions, such as thromboembolism  **Distributive Shock ** This type of shock occurs as a result of changes in the circulation with the volume of fluid remaining constant and there is no underlying heart condition. With distributive shock, the blood is sent to the wrong areas leading to potential deficiencies in oxygen or energy requirements in areas such as the brain, heart and lungs.  Causes of distributive shock include:  - **Endotoxic** - Endotoxins from bacteria cause increased permeability of blood vessels allowing the pooling of fluid within the tissues.  - **Neurogenic** - Inappropriate vascular tone (either vasoconstriction or vasodilation) can be caused by central nervous system injuries, anaesthesia or severe pain.  - **Anaphylactic** - Antigen-antibody reactions can cause histamine release, leading to increased permeability of blood vessels and a sudden drop in blood pressure.  **Treatment of Shock** Treatment of shock aims to support blood pressure, ensuring that tissues receive vital oxygen and energy. This can be done in a number of ways depending on clinical signs and veterinary preference.  Shock is a serious condition and the situation can deteriorate quickly. It is, therefore, important that the patient\'s clinical signs are monitored and changes identified. Cardiovascular parameters, such as mucous membrane colour, CRT, pulse rate and pulse quality, should be reviewed frequently. The recording of trends in physiological parameters is fundamental in assessing patient response to treatment and tailoring therapy as required. Ways we can treat shock include... - **Intravenous Fluid Therapy** - An important therapeutic priority in most forms of shock involves the administration of IVFT to resuscitate the intravascular compartment to maintain blood pressure and, thus, perfusion. This will often involve administration of rapid/bolus rates. In some cases this will need to be supplemented by other fluid and blood products, for example, to replace clotting factors. In cardiogenic shock, the administration of fluids may be contraindicated with therapy instead concentrated on diuretic and inotropic support. It is important, therefore, to liaise with the veterinary surgeon before assuming IVFT is required.  - **Oxygen Therapy** - With a reduced ability to provide oxygen to the tissues, supplementary oxygen can ensure that each red blood cell is fully saturated with oxygen. You should ensure that the patient remains calm when providing oxygen, as this can be counterproductive if the animal struggles or gets stressed by the face mask.  - **Corticosteroids** - The use of steroids in the treatment of shock is debatable and often depends on veterinary preference. The aim is to stabilise cell membranes and prevent fluid loss into the surrounding tissues, although there is some debate over the evidence of its efficacy in shock.  - **Analgesia** - Analgesia may be required as an adjunct to shock therapy, particularly if trauma or invasive surgery is involved. Consideration should be given to the choice of analgesic with the side effects of NSAIDs, particularly with regard to renal function, often contraindicating their use in shock.  - **Vasodilators** - The use of vasodilators in shock may be contraintuitive although, depending on the cause, they may be beneficial in distributive shock or to ease the work load in cardiogenic shock.  - **Intravenous Antibiotics** - Intravenous antibiotics may be appropriate in cases of endotoxic shock.  **Disseminated Intravascular Coagulopathy (DIC) ** If shock is not managed, the clinical signs can deteriorate to the point of life threatening circulatory failure. DIC is a secondary complication to prolonged shock, endotoxaemia, pancreatitis or hyperthermia.  As shock deteriorates into DIC, the clotting process throughout the body becomes over-reactive. This results in the utilisation of all clotting factors with generalised internal and external haemorrhage.  The condition can be treated but clinical signs associated with DIC should be quickly identified and treatment started promptly to increase the changes of survival.  Clinical signs are associated with the pathophysiology of excessive haemorrhage and thromboembolism.   Clinical signs of DIC include (often showing in the following order):  - Petechiae - pin prick haemorrhages (yellow circle in image). - Ecchymosis - merged petechiae so that it looks like bruising (white rectangle in image). - Petechiae and ecchymosis are most easily seen on the mucous membranes of the gums, conjunctiva or prepuce/vulva. These signs should also be looked for, however, in hair-free areas such as the abdomen, inner thighs and inner pinna.  - Haemorrhaging from eyes, ears or nose. - Multiple organ failure. Diagnosis of DIC focuses on platelet counts and clotting profiles, such as PT, aPTT and fibrin degradation products.  Treatment of DIC consists of supporting the body and the clotting ability of the patient:  - Treat the underlying condition - Maintain circulating volume (stop haemorrhage, IVFT, etc.) - Administration of anticoagulants, such as heparin (to prevent thrombus formation) - Administration of platelet rich plasma via transfusion Principles of Fluid Therapy: Aims of fluid therapy are... 1. To restore body water 2. To correct electrolyte balance 3. To replace haematopoetic components Types of fluid available are isotonic, hypertonic and hypotonic. Isotonic=If a solution has the same osmotic pressure as plasma it is described as ISOTONIC Hypertonic=If a solution has a higher osmotic pressure than plasma it is described as HYPERTONIC Hypotonic= If a solution has a lower osmotic pressure than plasma it is described as HYPOTONIC **Body Water ** On average, the water content of the body is approximately 60% of body weight. Body water content can vary with: **AGE** -- A young animal's body may contain 70-80% water, while in an older animal it may be as little as 50-55%.  **NUTRITIONAL STATUS** -- The proportion of fat to lean tissue can affect the body water:weight ratio as fat tissue contains a much smaller percentage of water than other tissue. Therefore, fluid requirements of an obese animal should be calculated on its ideal body weight. - Total body water= 60% of body weight - Extracellular fluid= 20% of body weight - Intracellular fluid= 40% of body weight - Interstitial fluid= 15% of body weight - Plasma= 5% of body weight Water losses: The amount of water lost from the body over a 24-hour period is... - 20ml/kg in insensible losses such as sweat and breathing. - 10-20ml/kg in faecal losses - 20ml/kg in urinary losses Therefore, the daily water requirement is 50-60 ml/kg/24 hrs **Urinary Losses ** Urine specific gravity can be measured to assess renal concentrating ability. Determination of Renal function is important as this may be a cause for fluid losses that will need to be compensated for, but also to ensure that any fluid given intravenously can be cleared effectively by the kidneys.  Normal urine output in the dog and cat is **1-2 ml/kg bodyweight/hour (24-48ml/kg/day)** Normal urine SG for dog is 1.015-1.045 and in a cat it is 1.020-1.060. **Isosthenuria** -- The urine specific gravity is the same as the glomerular filtrate/plasma (SG = 1.008), meaning that the kidneys are neither actively concentrating or diluting the filtrate in production of urine.  **Hyposthenuria** -- This describes decreased urine specific gravity (SG less than 1.015), suggesting that there may be renal insufficiency or the animal is polydipsic.   **Hypersthenuria** -- This describes increased urine specific gravity (SG more than 1.045), suggesting that the animal is dehydrated.  **Acid-Base Balance** The normal pH of extracellular fluid/plasma is 7.35-7.45 (slightly alkaline) and the body has several mechanisms to ensure it stays within this range - the acid/base balance.  Acidaemia/alkalaemia or acidosis/alkalosis describe serious states where the pH of ECF is abnormal. Enzymes and chemical processes will not work properly if the pH is outside the normal range.  There is a mechanism in place, called a **buffer response**, involving bicarbonate (HCO~3~).  There is free flow between the three areas, so that free hydrogen (H^+^) and bicarbonate (HCO~3~) can combine to make carbonic acid (H~2~CO~3~). Carbonic acid can be split to produce carbon dioxide and water. Equally, in the presence of carbonic anhydrase carbon dioxide and water can combine to make carbonic acid, which is broken down into hydrogen and bicarbonate. The direction of flow depends on what is happening within the body at any one time.    A diagram of a chemical reaction Description automatically generated The acid-base status in the body depends on many factors. The H^+^ or acid load is a result of the net effect of metabolic processes. The levels of bicarbonate are also regulated to match the amounts of acid being produced.  The kidneys can effect change in acid base balance through regulation of the excretion and resorption of H^+^ and HCO~3~^-^ ions. Amounts of CO~2~, which equates to carbonic acid levels, are regulated by minute volume by the respiratory centres of the brain. The lungs can retain and excrete CO~2~ (converted into acid) quite quickly, where the kidneys resorb or excrete HCO~3~ (base) over a more prolonged timescale.  An acidosis can occur due to too much CO~2~, loss of HCO~3~, or the intake or production of acids. Conversely, an alkalosis is usually the result of the gain of too much bicarbonate or the loss of too much CO~2~.  If an acidosis occurs, this will be neutralised by circulating bicarbonate. As the pH falls, the brain also stimulates alveolar ventilation to increase, and the CO~2~ levels will drop to less than normal. Finally, the kidneys will start to resorb bicarbonate over a number of days.  With an alkalosis, alveolar ventilation will decrease so that CO~2~ levels will rise, and HCO~3~^-^ excretion from the kidneys will begin.  **Respiratory Control** Respiration rate and tidal volume are controlled by chemoreceptors that detect changes in the H^+^ ion concentration of the blood.  **Respiratory Acidosis: ** Decreased respiration will cause CO~2~ (therefore carbonic acid) to be retained, thereby increasing H^+^ ions, lowering the pH and raising the acidity of the blood.   If the patient has metabolic alkalosis, hypoventilation will rebalance the problem. **Respiratory Alkalosis** Increasing respiration removes CO~2~ (lowering carbonic acid concentration), and thereby lowering H^+^ ions, increasing the pH and reducing the acidity of the blood. If a patient has metabolic acidosis, hyperventilation will rebalance the problem. **Renal Control** The kidneys control the levels of acid-base balance by controlling what is excreted in the urine. **Metabolic Acidosis** Increased loss of bicarbonate, such as with chronic small intestinal diarrhoea, leads to a relative increase in H^+^ and subsequent metabolic acidosis.  Renal correction of metabolic or respiratory acidosis involves increasing the excretion of H^+^ ions and/or decreasing the excretion of bicarbonate ions to rebalance the ratio between H^+^ (acid) and bicarbonate (alkali).    **Metabolic Alkalosis** Increased loss of hydrochloric acid (HCl), such as with chronic vomiting, leads to a relative decrease in H^+^ ions and subsequent metabolic alkalosis.  Renal correction of metabolic or respiratory alkalosis involves increasing the excretion of bicarbonate and/or decreasing the excretion of H^+^ ions to rebalance the ratio between H^+^ (acid) and bicarbonate (alkali).  Assessing fluid requirements: Assessing fluid requirements involves ensuring all losses are accounted for. This can involve a number of steps... Identify type of fluid lost- Water losses can be primary or mixed:  - **Primary water losses **include reduced water intake through illness, neglect or being trapped in sheds, etc. where there is no access to water; or through increased water loss such as panting or prolonged anaesthesia.  - **Mixed losses** involve the loss of water and electrolytes through conditions such as vomiting/diarrhoea or draining wounds/burns; or through extensive haemorrhage. History of clinical signs- A clinical history enables an accurate assessment of fluid deficits to be made; i.e. how many days has the dog had diarrhoea? Clinical signs are a useful tool for *identifying*dehydration, such as the retraction of the third eyelid in cats as the eyes sink with contraction of the suborbital fat pads. However, clinical signs are not always an *accurate* means of assessing dehydration as other factors, such as increased or decreased body fat, can affect the skin elasticity. Diagnostic tests- Packed cell volume (PCV) can be used to provide a more objective method of assessment.  However, when using this method rarely is the normal PCV of the patient known and, therefore, an estimate of 45% for the dog and 35% for the cat is used. For every 1% increase in the PCV above the normal percentage, a fluid loss of approximately 10ml/kg/bodyweight has occurred (**kg x difference in % x 10**). This method is unreliable in anaemia as the PCV is a comparison between plasma and RBCs and, consequently, will not be an accurate assessment of dehydration in this situation. Calculating fluid requirements- When calculating fluid requirements, you should calculate: 1. **The fluid deficit** - based on the clinical history **OR **the clinical assessment (% dehydrated)/diagnostic assessment (PCV) 2. **The ongoing losses** - such as episodes of vomiting/diarrhoea or estimated loss from burns/wounds 3. **The maintenance requirements** - based on water losses, such as urinary/faecal and insensible losses, if not eating/drinking to replace these **Types of Fluid** As well as considering the volume of fluid lost, we should also determine what type of fluid has been lost. The best option is generally to replace *\'like with like*\' so that we match primary water losses, mixed water losses or blood products to the type of replacement fluid administered.  These include crystalloids, colloids and blood products. Crystalloids= Crystalloid fluids readily pass through cell membranes, not staying in the circulation very long but rapidly equalising into the ECF within about 20 mins. Crystalloids are readily excreted in urine if renal function is normal.  Crystalloid fluids are generally isotonic, but can be hypo- or hypertonic. Colloids= Colloids contain larger molecules and remain within the circulation for increased periods of time. They act to increase the plasma's osmotic pressure, drawing fluid from the surrounding tissues into the circulation and becoming a *plasma expander* to maintain circulating volume. Colloids are hypertonic solutions, are used in hypovolaemic shock.  Blood products= Blood products can be used to replace whole blood or components, such as plasma or platelets, as required. **Whole Blood - **This fluid is indicated for acute or chronic haemorrhage, in cases of anaemia or for patients with clotting or platelet deficiencies. Whole blood can be separate to provide blood fractions, such as **plasma**, **platelet rich plasma**, or **platelets**.Autotransfusion can be used where the animal\'s blood is removed prior to surgery and transfused when required.  The route of administration will depend on the species and the degree of dehydration.  - **Oral** - This method is only used with mild dehydration due to the restriction of volumes that can be given and is contraindicated if the patient is vomiting or is comatose.  - **Subcutaneous **-- This method is only used to maintain hydration due to the restriction of volumes that can be given and the changes in peripheral perfusion once the animal becomes dehydrated.  - **Intraperitoneal **-- This method must have fluids warmed to body temperature to prevent shock as the fluid rapidly cools the internal organs.  - **Intraosseus** -- This method is good for neonates and exotics where intravenous access can be challenging. - **Intravenous **-- This is the most common method due to the direct access to the circulation, allowing adequate volumes to be given.  **Volume and Rate of Infusion** The volume of fluid to be replaced should be calculated following a physical examination and/or the completion of laboratory tests.  The calculated amount is administered over the first 24 hours, often with half of the deficit requirement being administered during the first 6 hours.  In the case of severely shocked patients, half of the requirements can be given at a greater rate, i.e. within 2 hours, and it may be necessary to place two IV lines in order to administer large amounts. In cases of very high rates of administration, a bolus may be administered for 15 minutes initially, followed by a reassessment of perfusion and subsequent adaptation of the treatment plan as appropriate.  The amount of colloid given should be 1/12th of the deficit or to the maximum rate. **The maximum rate of infusion of a crystalloid is:** **  DOGS = 60-90 ml/kg/hr ** **  CATS = 40-60 ml/kg/hr** **The maximum rate of infusion for a colloid is:** **  DOGS = 10-20 ml/kg/hr** **  CATS = 8-12 ml/kg/hr** **Over Administration** Administering fluid too rapidly can result in the circulatory system becoming overloaded. This is more likely to occur in smaller patients, cardiac patients and renal patients. Over administration of colloid can result in right sided heart failure (elevated central venous pressure would indicate this) and can eventually lead to congestive heart failure. Assessment of clinical signs is important to identify over-infusion: Cardiovascular clinical signs of over-infusion- Auscultation,Electrocardiogram (ECG), Mucous Membrane Colour, Peripheral Pulse Quality, Arterial Blood Pressure, Central, Venous Pressure Other clinical signs of over-infusion- Tachypnoea, Serous Nasal Discharge, Restlessness, Rise in Temperature, Adventitious Chest Sounds (crackles)  **Central Venous Pressure (CVP)** CVP is used to determine the pressure within the caudal vena cava or right atrium. This gives a direct impression of the ability of the heart to distribute the fluid within the cardiovascular system. Rapid administration of fluid or cardiac insufficiencies will lead to increased CVP.