Anaesthesia Emergencies Pathophysiology Notes PDF

BURNS PATHOPHYSIOLOGY Hypovolaemia (Low blood volume) Cytokines and In ammatory mediators cause uid to leak out of blood capillaries into tissues, causing oedema. Loss of electrolytes such as potassium and sodium & albumin (that help the uid stay inside blood vessels) are lost in the burned...

BURNS PATHOPHYSIOLOGY Hypovolaemia (Low blood volume) Cytokines and In ammatory mediators cause uid to leak out of blood capillaries into tissues, causing oedema. Loss of electrolytes such as potassium and sodium & albumin (that help the uid stay inside blood vessels) are lost in the burned area contributes to hypovolaemia. All of these factors which contribute to hypovolaemia then lead to Metabolic Acidosis. WHY? Loss of blood volume = loss of oxygen-carrying capacity = lactic acid buildup = metabolic acidosis. Heart rate will increase to try and compensate for loss of O2 and to maintain cardiac output due to loss of blood volume. Peripheral and Splanchnic Vasoconstriction Stress response of body (Release of noradrenaline and catecholamines) causes vasoconstriction from limbs (Peripheral) and intestines and stomach (Splanchnic) to draw blood to major organs such as brain, lungs and heart. Hypovolaemia ( uid loss) causes the body to maintain adequate blood pressure by drawing blood to major organs. Vasoconstriction of peripherals can cause low perfusion in tissues = hypoxia. Vasoconstriction in splanchnic regions can a ect the metabolism of drugs given. The patient would have low blood pressure due to hypovolaemia and loss of uids. IMPORTANT TO NOTE: Vasodilation would occur in essential organs such as the brain, heart and lungs to achieve maximum perfusion. Metabolic Changes = Metabolic Acidosis Severe burns trigger the release of cytokines and in ammatory mediators to try and repair damage quickly = which increases heart rate, oxygen consumption and metabolism (hypermetabolism). Catabolism: Breakdown of muscle and fat at an accelerated rate to provide nutrients and energy for tissue repair. Muscle breakdown = protein loss = hypermetabolism. Hypermetabolism then causes an increased demand for ATP and oxygen-enriched blood to maintain the accelerated repair process. Respiratory rate increases: due to the body’s need for more oxygen and to expel excess carbon dioxide from hypermetabolism. Metabolic Acidosis: Occurs when there is insu cient oxygen to maintain hypermetabolism demands = anaerobic metabolism creates lactic acid buildup in blood = metabolic acidosis. Insulin Resistance and Increased Glucose Production = Hyperglycaemia Why? Catecholamines interfere with insulin binding capability (insulin allows glucose to enter cells). Faulty insulin = increased dispaced glucose in the bloodstream rather than cells. The liver will rst use up its glycogen stores (glycogenosis); once used, it will produce glucose using non- carbohydrate sources such as amino acids, lipids and lactate (gluconeogenesis). The liver won't stop producing glucose due to the release of catecholamines and cortisol. Usually, when blood glucose rises, insulin will increase and tell the liver to stop producing glucose, but in the case of burns, it will not. These factors then lead to Hyperglycaemia due to decreased glucose uptake via insulin resistance. Hypothermia: Due to loss of thermoregulators in dermis. Lethal Triad: Hypovolaemia, Metabolic Acidosis, Hypothermia = Death. fi fl fl ff fl ffi fl fl fl Burns Treatment: Airway, Breathing, and Circulation: Airway: If the patient has burns to the face or neck, there may be airway compromise due to swelling. If there's concern about airway obstruction, intubation may be needed. Breathing: Administer oxygen if the patient shows signs of respiratory distress, especially if the burn involves inhalation injury (e.g., from smoke or chemical fumes). Circulation: Ensure adequate perfusion by assessing blood pressure and heart rate. Establish IV access to provide uids, and monitor for signs of shock (like hypotension, tachycardia, and low urine output). Fluid Resuscitation: Burn injuries result in uid loss due to capillary leak and increased permeability of blood vessels. This leads to hypovolemia. Parkland Formula: The most common method for calculating uid requirements in burn patients. Crystalloid uids (Hartmanns): typically used for uid resuscitation in the early hours after the burn. Colloids (e.g., gelofusion): may be used later to help maintain blood volume. Monitoring uid status: Urine output is a key indicator of adequate resuscitation (targeting 0.5-1 mL/kg/hr in adults). Early Enteral Feeding: Helps the body get the necessary nutrition it needs due to hypermetabolic demands & also will aid in wound healing, immune function and tissue repair. Maintains gut integrity following prolonged periods of inactivity and decreases the likelihood of leaky gut, which can cause infection and sepsis. fl fl fl fl fl fl ANAPHYLAXIS PATHOPHYSIOLOGY Grade 1: Local Reaction (Redness, swelling) Grade 2: Mild-Moderate Reaction (Vomiting, abdominal pain, ushing, angioedema) Grade 3: Severe Systemic Reaction ( Systemic with cardiovascular -/+ respiratory response: wheezing, stridor, low blood pressure, cardiac arrest) Allergic Antibody: Immunoglobulin E (IgE) Exposure to allergen (i.e, dust): White blood cells mature into plasma cells and generate speci c IgE against allergen. IgE circulates bloodstream and binds to tissue mast cells with IgE receptors. Mast cells hold histamine and are now sensitised to allergen. Exposure to allergen = allergen binds to mast cells = release of in ammatory mediators such as histamine, prostaglandin and cytokines. Histamine = Vasodilation of blood vessels (low BP) increased vascular permeability ( uids leaking out of blood vessels) (oedema, hives) and smooth muscle contraction (bronchoconstriction) (coughing, wheezing). Prostaglandins = Contribute to in ammation and bronchoconstriction. Cytokines = Stimulate more IgE production and mast cell response, which further increases in ammation and enhances allergic response. Stroke Volume X Heart Rate = Cardiac Output Cardiac Output X Systemic Vascular Resistance = Blood Pressure Capillary Permeability due to Histamine Release = Loss of Blood Volume = Loss of Oxygen Carrying Capacity = Increased CO2 = Increased Respiratory rate. Bronchoconstriction due to Histamine and Prostaglandin release = More resistance breathing, use of accessory muscles = Lack of di usion of oxygen into bloodstream. Prostaglandins increase swelling and airway oedema with Mucus Production via Goblet cells, increasing respiratory distress = Tachyapnea is used to try and compensate for lack of oxygen. Excess CO2 in blood and inadequate gas exchange = Respiratory Acidosis. Hypoperfusion and Hypovolaemia = Myocardial Damage and Ventricular Dysfunction. Respiratory acidosis, hypotension, hypoxia, and hypovolaemia cardiac arrhythmias can lead to cardiac arrest. Rash = Due to vascular permeability. Treatment: Immediate IM Bolus of Adrenaline (1:1000). (Bronchodilator for airway (Beta Response)) Vasoconstrictor for Low Blood Pressure (Alpha Response) ALSO Decreases Vascular Permeability, which reduces Oedema and further uid loss. Inhibits the release of more histamine. Increases CARDIAC OUTPUT. High Flow O2: To treat respiratory distress and allow for gas exchange. Treat Respiratory Acidosis and hypoxia. Crystalloid Fluid Bolus: To treat Hypovolaemia and Increase Blood Pressure. CONSIDER: ENDOTRACHEAL INTUBATION IF AIRWAY IS COMPROMISED DUE TO OEDEMA AND BRONCHOCONSTRICTION. fl ff fl fl fl fl fi fl LOCAL ANAESTHETIC SYSTEMIC TOXICITY (LAST) PATHOPHYSIOLOGY Takes place within 10 mins- 1hr after administration. Blocks pain receptors from sending signals to the brain. DIFFERENT LA’S HAVE DIFFERENT DISSOLVING RATES = FASTER TOXICITY. Key Enzyme: Sodium (Na+) channels are blocked by the LA; this interferes with signals to the brain. Na+ carries an electrical charge responsible for muscle contraction and nerve impulse. No Na+ = arrhythmias- as it prevents early depolarization (allowing the heart to rest between contractions) LAST occurs when LA anaesthetic reaches a level that a ects the heart and brain. This can happen either by: Injection directly into blood vessel. Overdose of LA Injecting near a vascularised area. How does it happen? LA absorbed into circulation- binds to plasma- plasma becomes saturated = systemic circulation toxicity. LA inhibits oxidative phosphorylation (in mitochondria), which is needed to create ATP No ATP = Anaerobic Metabolism and unable to displace hydrogen ions from blood = metabolic acidosis. Reduction in SVR (WHICH NEEDS ATP) VASOPRESSORS AND INOTROPES INEFFECTIVE NO HYPERVENTILATION TO EXPEL EXCESS CARBON DIOXIDE AS ATP IS NEEDED. EFFECT ON THE BRAIN LA drugs cross the blood-brain barrier and block nerve impulse signals. Initially causes CNS EXCITATION: Fasciculation/ seizures/ numbness around the mouth. As it worsens, it can cause respiratory depression and apnea. Symptoms: Tinnitus, tingling, slurred speech, and loss of consciousness. EFFECT ON THE HEART Blocks ion channels which reduces the heart's cardiac conduction: Leads to BRADYCARDIA, AV BLOCK, PROLONGED PR INTERVAL AND WIDENED QRS. LA reduce SVR (DUE TO NO ATP), leading to a LOW BP. This and BRADYCARDIA LEAD TO REDUCED CARDIAC OUTPUT. The heart will try and compensate for low CO via tachycardia but ultimately will progress to arrhythmias, bradycardia = cardiac arrest. LAST TREATMENT STOP LA ADMINISTRATION USE ABC APPROACH Is the patient spontaneously breathing?BP? SPO2? 20% INTRALIPID FLUID BOLUS (MAX DOSE =12ML/KG) Draws LA out = increase SV = Increased BP IV ACCESS AND FLUID RESUSCITATION To support low BP BENZODIAZEPINES FOR SEIZURES CARDIAC ARREST TROLLEY Amiodranone for arrhythmias IF CARDIAC ARREST OCCURS GIVE SMALLER ADRENALINE DOSE (Too much can worsen arrythmias) ff MALIGNANT HYPERTHERMIA PATHOPHYSIOLOGY WHAT IS IT? A life-threatening reaction to anaesthetic gases and succinylcholine. Skeletal muscle contracts repeatedly, producing heat, excessive CO2, and tachycardia. NORMAL MUSCLE CONTRACTION: Action Potential (for muscle to move)- electrical impulse releases acetylcholine- causes excitement (depolarisation) once it enters receptor- depolarisation releases CALCIUM from the sarcoplasmic reticulum (WHERE CALCIUM IS STORED)- Ryonodine Receptors (RyR1) trigger release of calcium- Calcium binds to troponin (between actin and myosin ligaments)- troponin is pulled away & ligaments rub together causing contraction. ATP AND O2 IS USED UP BY STOPPING LIGAMENTS CONTRACTING, & CALCIUM IS PUMPED BACK INTO SR. PRODUCING HEAT FROM CONTRACTION. MH CHANGES IN CONTRACTION: Genetically altered RyR1 Receptors Receptors become hypersensitive once triggered by gases or sux & trigger massive, uncontrolled calcium release into the cytoplasm. Too much calcium = too much muscle contraction = heat = HYPERTHERMIA. Too much calcium will prevent troponin from re-sheathing ( which allows muscles to relax) Muscle bres will use up O2 and ATP rapidly, creating CO2 and heat as by product, causing cell death and rhabdomyolysis (breakdown of muscle tissues). RHABDOMYOLYSIS: BREAKDOWN OF SKELETAL MUSCLE Muscle death = release of MYOGLOBIN, TROPONIN AND POTASSIUM into the bloodstream. Myoglobin can obstruct renal tubules and impair renal blood ow, causing ACUTE KIDNEY INJURY. This leads to HYPERKAELAEMIA (high potassium levels) as kidneys can't excrete potassium e ciently. HYPERKAELAEMIA LEADS TO EXTRASYSTOLES ON ECG. HYPERCARBIA & RESPIRATORY ACIDOSIS: ATP demand increases due to excessive muscle contraction/ hypermetabolism = production of CO2. Capnograph will show an increase in CO2 Resistant to hyperventilation and PEEP. GA without paralysis = patient increases depth and rate of spontaneous respiration. Excess CO2 = Respiratory Acidosis. LACK OF ATP AND OXYGEN INHIBITS BODY FROM EXPELLING CO2 EFFECTIVELY. HYPOXAEMIA & TACHYCARDIA: Excessive production of CO2 makes blood PH acidic—demand for O2 increases, leading to metabolic acidosis. Tachycardic from hypermetabolism as body tries to meet O2 demands. HYPERTHERMIA: OCCURS AFTER TACHYCARDIA AND HYPERCARBIA Rises by 1 degree Celcius every few mins Product of excessive muscle contraction. Treatment: Disconnecting from anaesthetic machine with o2 cylinder. CONSIDER TIVA. Replace lters and circuits, and add activated charcoal lters. 100% FiO2 Administer DANTROLENE Muscle relaxant to stop contraction COOLING MEASURES SODIUM BICARBONATE: TO CORRECT METABOLIC ACIDOSIS. CATHETER TO MEASURE URINE OUTPUT Insulin to treat hyperkalaemia ( moves potassium back into cells) & calcium gluconate to stabilise arrhythmias ( safer than calcium chloride) fi fi fi fl ffi SEPSIS PATHOPHYSIOLOGY MAJOR HAEMORRHAGE PATHOPHYSIOLOGY