Anaesthesia Monitoring PDF

ANAESTHESIA MONITORING MIMV 3rd year – 1st semester TP 04 September 2024 Ricardo Felisberto, DVM, Dipl. ECVAA, MRCVS  INTRODUCTION Why monitoring animals under anaesthesia?: To ensure maintenance of physiological functions To ensure an adequat...

ANAESTHESIA MONITORING MIMV 3rd year – 1st semester TP 04 September 2024 Ricardo Felisberto, DVM, Dipl. ECVAA, MRCVS  INTRODUCTION Why monitoring animals under anaesthesia?: To ensure maintenance of physiological functions To ensure an adequate anaesthesia depth To improve patient safety (e.g., horses high anaesthesia-related mortality) Horses: 1 death in 100 cases Dogs: 1 death in 1800 cases Cats: 1 death in 900 cases Personnel safety (by administering appropriate analgesia and sedation) Complete anaesthesia records as they are legal documents  INTRODUCTION What should be monitored?: Central nervous system (CNS) Cardiovascular system (CVS) Respiratory system Temperature Neuromuscular function Renal function Metabolic status (haematological and biochemical variables) Coagulation status  CNS MONITORING Assessment of reflexes: Palpebral: check both eyes if possible; if you over-check reflex becomes refractory. Corneal: present until deep anaesthesia. Gag / jaw tone: laryngeal and pharyngeal reflexes may persist in pigs and cats until deep anaesthesia. Limb withdrawal reflexes: important in rabbits (too light, spontaneous limb movement) Perineal: important in horses if can’t have access to the face Righting: often used for exotics (light anaesthesia = maintenance of righting reflex) Eye movement / position / lacrimation: Dogs, cats, cattle: eye position ([light] central → ventromedial rotation → central [deep]), palpebral reflex, nystagmus and lacrimation = indicate anaesthesia depth. Horses: maintain spontaneous slow palpebral contraction even at deep anaesthesia, but globe position is unreliable.  CNS MONITORING Autonomic nervous system activity monitoring: Heart rate, arterial blood pressure: Nociception can stimulate the sympathetic nervous system: Tachycardia and hypertension But can also induce a vagal reflex = bradycardia and hypotension In horses, if there is a response to nociception, we will mainly see hypertension, due to increased stroke volume and not heart rate. Parasympathetic tone activity (PTA) monitoring: If there is predominance of parasympathetic tone = each inspiration is associated with a higher heart rate which decreases the R – R interval momentarily, which lead to a higher heart rate variability → PTA is high. If there is predominance of sympathetic tone = the heart rate increases but R – R interval is more similar, leading to lower heart rate variability → PTA is low. 0-100 range: 70: predominant parasympathetic tone. It relates to analgesia-nociception balance during anaesthesia.  CNS MONITORING Electroencephalography: Records the electrical activity of the cortical brain using electrodes over the scalp. Can be affected by hypoxia; hypercapnia; severe hypocapnia; hypothermia; hypotension. It is composed by different wave frequencies: δ: 13Hz Consciousness: predominant low amplitude and high frequency waves (more α and β). Anaesthesia: predominant high amplitude and low frequency waves (more θ and δ). Analysis of the correlation between the different frequencies at different anaesthesia depth → Bispectral index (BIS) which gives a number from 0 (isoelectric activity) to 100 (awake). Ideal anaesthetic depth = BIS 60% Not yet validated in animals due to different head shape and bone thickness compared to humans.  CVS MONITORING The main goal of the CVS system is to guarantee tissue oxygen delivery (DO2). Monitoring of the CVS system is essential so we can help maintaining DO2. Several factors can influence the DO2 but we can divide them into 3 major ones: Cardiac output Arterial oxygen content Oxygen extraction Of these, we can only measure some of the subfactors in a clinical setting. Intravascular blood volume Cardiac capacity (pericardial disease / myocardial disease) Systemic Venous vascular PO2 resistance Preload Oxygen Oxygen Arterial blood pressure extraction consumption Afterload Stroke Metabolic Tissue rate volume Myocardial Cardiac oxygen contractility output delivery Heart rate Temperature and rhythm Thyroid hormone levels Arterial blood Catecholamines oxygen content Venous admixture (V/Q mismatch; shunt) Arterial Diffusion impairment Haemoglobin saturation with O2 PO2 Haemoglobin concentration (Anaemias) Dyshaemoglobins: Methaemoglobin; Inspired O2 Alveolar carboxyhaemoglobin; thalassaemia; percent PO2 sickle haemoglobin Tidal Other volume Alveolar inspired ventilation gases Breathing rate Physiological dead-space Atmospheric Apparatus dead-space pressure  CVS MONITORING CO = HR x SV ABP = HR x SV x SVR DO2 = CO x CaO2 CaO2 = [Hb] x 1.34 x SaO2 + 0.003 x PaO2 Why is it important to monitor the CVS?: Anaesthetic agents depress the CVS and respiratory function; both essential to maintain the DO2. They do it by decreasing myocardial contractility; reduced systemic vascular resistance = hypotension and lower cardiac output. We don’t normally measure CO in clinical setting; the second best is the ABP, which should be maintained 60 – 70 mmHg to allow organ perfusion and autoregulation mechanisms active.  CVS MONITORING What happens after acute haemorrhage?: Hypovolaemia = ↓ venous return = ↓ preload = ↓ cardiac output = hypotension. Immediate response (seconds): hypotension detected by low-pressure mechanoreceptors in the right atrium, the arterial baroreceptors and carotid body and aortic arch → ↑ Sympathetic tone = ↑ SVR + ↑ HR + ↑ myocardial contractility. Vasoconstriction = reduced gut and skin perfusion and ↑ brain, heart, lungs, kidneys perfusion and maintenance of autoregulation of blood flow. Early response (minutes to hours): restoration of blood volume (transcapillary fluid movement) → ↑ renal retention of Na+ and H2O, mainly due to: Activation of RAAS due to ↑ sympathetic tone. ↓ release of Atrial Natriuretic peptide due to less right atrium stretch. ↑ ADH release due to hypovolaemia and ↑ plasma osmolarity. ↑ cortisol release. Late response (hours to days): restoration of blood volume by oral intake of water and renal reabsorption of electrolytes and water + new RBCs production (within 4 to 6 days).  CVS MONITORING What can we monitor?: Heart rate; rhythm monitoring: electrocardiography Palpation of the apex beat: palpation Auscultation of heart sounds: precordial stethoscope; oesophageal Peripheral pulse palpation (quality): palpation Femoral (all animals); brachial arteries (birds, large animals); lingual (dogs); palatine and transverse facial (horses); mandibular (horses, ruminants, pigs); caudal auricular (all animals); dorsal pedal (dogs, cats); median coccygeal (horses, cattle). Pulse pressure is ↑ if there is ↑ SAP and DA difference (pulse strong – bounding) = in PDA and aortic valve insufficiency. If we can stop the arterial flow easily with compression = hypotension. Transoesophageal echocardiography: evaluate heart performance in real-time and cardiac output. 𝑆𝐴𝑃 −𝐷𝐴𝑃 Arterial blood pressure: MAP = + 𝐷𝐴𝑃 3 MAP is the most relevant variable compared to SAP and DAP, because it represents the perfusion pressure of the organs (essential for DO2).  CVS MONITORING Electrocardiography: Essential for accurate diagnosis of arrhythmias. Assesses the electrical activity of the heart in terms of rate and rhythm, but not tell if the heart is beating. Pulseless electrical activity (there is electrical activity, but the heart is not beating) – cardiac arrest rhythm. Requires at least 3 electrodes positioned in a triangular shape (e.g., Left forelimb - yellow; Right forelimb - red; Left hindlimb - green). Place it before induction (+ NIBP)! (↑ vagal tone during endotracheal intubation may lead to CPA)  CVS MONITORING Arterial blood pressure: Non-invasive: Sphygmomanometer; oscillometry; high definition oscillometry; plethysmography. Measures MAP and estimates SAP and DAP Invasive (gold-standard): measures SAP and DAP and calculates MAP Sphygmomanometer: Uses an inflatable cuff, and its internal pressure is measure by a mercury manometer The cuff is inflated until blood flow to the distal limb is occluded. The cuff is the deflated slowly (2 mmHg / beat) and the pulsatile blood in the artery distal to the cuff is detected by palpation, auscultation or doppler. Using doppler: pressure in cuff at which blood flow returns = SAP in dogs; MAP in cats  CVS MONITORING Arterial blood pressure: Oscillometry: Automated version of sphygmomanometer. The cuff width should be 40% of the circumference of the limb: If the cuff is too tight: gives falsely high ABP measurement If the cuff is too loose: gives falsely low ABP measurement Cuff should be placed in a limb at the level of the heart: If lower than the heart: gives falsely high ABP measurement If higher than the heart: gives falsely low ABP measurement The device detects the return to blood flow by changes in oscillation of the cuff pressure: Maximal rate of increase in oscillation size = SAP Maximal oscillation amplitude = MAP Maximal decrease in oscillation size or disappearance of oscillations = DAP High definition oscillometry: High sensitivity devices Have a screen that shows the changes in pressure as it is measured. Plethysmography: Can measure pulsatile blood flow and display it as a waveform. It does not give a number but displays pulse strength. TO BE TRUSTED?  CVS MONITORING Arterial blood pressure: Invasive: Requires arterial catheterization Connect a saline-filled non-compliant system Non-compliant connected to a pressure transducer which is tube Transducer then connected to the monitor to give the ABP measurements. Most peripheral arteries will have distal pulse Cable to amplification (overestimation of SAP, connect to underestimation of DAP, but MAP is similar to the monitor that of aorta) Important that the system is zeroed to atmospheric pressure and levelled to the heart – for more accurate measurements. Connection to arteria catheter Bubbles, blood clots, excessively long system, and too narrow catheter will interfere with the measurements.  CVS MONITORING Why is it important to measure MAP and to maintain it within normal range? Because at a specific range of blood pressures (60 to 160 mmHg) the blood flow of the organ (brain, kidney, heart) is independent of blood pressure. But outside this range it becomes directly proportional to blood pressure.  CVS MONITORING Why don’t we measure MAP invasively in all cases?: Expensive equipment Requires training for arterial cannulation Trauma of the artery Haematoma formation Infection Thromboembolism Necrosis  CVS MONITORING Central venous pressure (CVP): Measures pressure inside cranial vena cava or right atrium Indicator of volume status Indicates how well the heart copes with fluid therapy Best used as an indicator to stop fluids (e.g., if sudden increase of CVP = stop fluids as the heart will not cope with further fluids) What influences the CVP?: Heart compliance (chamber filling) Stage of heart cycle Intrathoracic pressure Intra-abdominal pressure Position (standing or head down)  RESPIRATORY SYSTEM Observation: Respiratory rate; rhythm; mucous membrane colour Thoracic wall movement; reservoir bag movement; unidirectional valves movement Water vapour condensing in the ETT Capnography: Respiratory rate; End-tidal carbon dioxide Spirometry: Tidal volume; airway pressures; minute ventilation  RESPIRATORY SYSTEM Assessment of ventilation: Gold-standard is arterial blood gas analysis Less invasive and continuous method = capnography Capnography: End-tidal CO2 (EtCO2) reflects PaCO2. EtCO2 is usually diluted by the anatomic dead-space, thus giving a typical difference of PaCO2 – EtCO2 of 3 to 5 mmHg (Horses can be 10 – 20 mmHg difference, due to large V/Q mismatch and larger anatomical dead-space). PaCO2 dogs and horses = 35 – 45 mmHg; PaCO2 cats = 27 – 35 mmHg. < 25 mmHg = ↓ cerebral blood flow = ↓ cerebral ischaemia 45 to 60 mmHg = permissive hypercapnia; acceptable as it stimulates the sympathetic tone and maintains spontaneous ventilation. > 60 mmHg = acidaemia; direct negative inotropy; arrhythmogenic.  RESPIRATORY SYSTEM Capnography: Sidestream: Gases are withdrawn from the breathing system at 200 mL/min (main not be suitable for low flow anaesthesia or very small patients, especially if the analysed gases are not returned to the breathing system) Delay between sampling site and reading on the monitor Less bulky; can have the analyser away from the patient; water condensation is trapped in a water trap Mainstream: Sensor is attached between the ETT and the breathing system Adds bulk to the system and apparatus dead-space, may get obstructed with blood clots or secretions No delay between gas sampling and the reading on the monitor Warms gases to avoid water condensation in the sensor Values may be more accurate than sidestream. Doesn’t require analysed gases to be scavenged  RESPIRATORY SYSTEM Capnography: Monitoring capnography tells us about: Metabolism: High metabolic rate = ↑ CO2 production (hyperthyroidism; phaeochromocytoma; hyperthermia; malignant hyperthermia) Ventilation: If alveolar ventilation is ↑ = ↓ PaCO2 and ETCO2 Circulation: If lower cardiac output = less pulmonary perfusion = ↓ ETCO2 (typical in cardiopulmonary arrest); successful cardiopulmonary resuscitation with return of spontaneous circulation = sudden ↑ ETCO2. Equipment function: If ETT is in the airway and patent (gold-standard to check if ETT is in the trachea). If ETT is too long (by increased apparatus dead-space and CO2 rebreathing). If there is a disconnection of the ETT or there are leaks in the system Soda lime exhaustion (CO2 rebreathing). One-way valves working (CO2 rebreathing). Not enough FGF in non-rebreathing systems (CO2 rebreathing).  RESPIRATORY SYSTEM ETCO2 values interpretation: If it is High: Rebreathing of ETCO2: ↑ dead-space (too long ETT; exhausted soda lime). Delivery of ETCO2 with the fresh gases. ↑ ETCO2 production: Light general anaesthesia Hyperthermia / malignant hyperthermia Hyperthyroidism Phaeochromocytoma ↓ ETCO2 excretion: Hypoventilation (obstruction, muscle relaxation, central respiratory depression) Endobronchial intubation: Bypasses one lung and the reduced tidal volume generated may lead to hypoventilation  RESPIRATORY SYSTEM ETCO2 values interpretation: If it is Low: ↑ CO2 excretion: Hyperventilation Animal too light ↓ CO2 production: ↓ metabolic rate Hypothermia Hypothyroidism ↓ cardiac output / CPA: Decreased pulmonary perfusion Disconnection of the ETT / occluded with secretions or blood clot; leaks  RESPIRATORY SYSTEM ETCO2 waveform interpretation: O → P: start of expiration (anatomical dead-space gases). P → Q: mixture of anatomical dead-space and alveolar gases. Q → R: plateau, exhalation of alveolar gases. R: end-tidal CO2 measurement; CO2 partial pressure at the end of expiration represents the alveolar partial pressure of CO2, which represents the PaCO2. R → S: Inspiration. α-angle: indicates the V/Q mismatch of the lung. It ↑ if there is obstructive lung disease (asthma; bronchospasm) (because dead-space gases takes longer to be exhaled). β-angle: indicates the extent of rebreathing.  RESPIRATORY SYSTEM Bronchospasm (shark-fin shaped) Hyperventilation Hypoventilation  RESPIRATORY SYSTEM Apnoea / drop in cardiac output / CPA  RESPIRATORY SYSTEM CO2 rebreathing Cardiogenic oscillations Curare cleft  RESPIRATORY SYSTEM Sampling leak Lung emphysema (downward sloping plateau phase due to destruction of alveolar capillary membranes and reduced gas exchange)  RESPIRATORY SYSTEM Assessment of oxygenation: Gold-standard is arterial blood gas analysis (PaO2) Venous PO2 (PvO2) indicates how much oxygen remains in the venous blood after tissue perfusion. Depends on: uptake from the lungs; tissue perfusion; peripheral oxygen extraction; reflecting the CVS and respiratory systems function. Pulse oximetry: Non-invasive and continuous measurement of the degree of saturation of the haemoglobin with oxygen (SpO2). Normal SpO2: 95 – 100% → PaO2 > 80 mmHg Severe Hypoxaemia SpO2: 90 mmHg), there will be only small changes on the SpO2. As we administer high FiO2 (100%) = PaO2 is going to be high (500 mmHg) (PaO2 = 5 x FiO2) If atelectasis (V/Q mismatch) develops during PaO2 (mmHg) SpO2 (%) general anaesthesia, the SpO2 will only indicate a 40 70 problem when PaO2 is only bellow 90 mmHg 60 90 (delayed indicator of oxygenation problem) 80 95  RESPIRATORY SYSTEM Pulse oximetry: Uses 2 mechanisms: Pulse photoplethysmography: The changing volume of the tissue bed due to arterial pulsation is measured by light absorption. Spectrophotometric oximetry: Oxyhaemoglobin (OHb) and Deoxyhaemoglobin (DHb) absorb different wavelengths of light (different absorption spectra): OHb: red because absorbs blue light and reflects red light. DHb: blueish because absorbs red light and reflects blue light. Beer-Lambert law: how light absorbance increases with a higher concentration of the absorbing substance in a medium (Beer) and also increases with the path length for light to travel (Lambert). Absorbance = e x L x C e – molar extinction coefficient; L – pathway length; C – concentration of the absorbing substance.  RESPIRATORY SYSTEM Pulse oximetry probe: Emitting diode (LED): shine light of the red and infrared wavelengths at alternating frequency. Receiver: receives the light that was not absorbed and works out the difference (emitted – received). Machine evaluates the ratio of the red and infrared light absorbed and discounts the constant part, only doing the ratio for the pulsatile input. The ratio gives Haemoglobin saturation with oxygen. OHb: absorbs more light at 940 nm (infrared light) DHb: absorbs more light at 660 nm (red light) Masimo pulse oximetry technology: Uses more wavelengths that allow distinction of different haemoglobin species (carboxyhaemoglobin; methaemoglobin)  RESPIRATORY SYSTEM Interferences: Algorithm of most pulse oximeters is for humans. Signal detection is affected by: Hypotension Vasoconstriction Skin pigment Hypovolaemia Hypothermia a2 agonists Bradyarrhythmias Venous pulsations Carboxyhaemoglobin (erroneously high SpO2) Methaemoglobin (erroneously low SpO2) Anaemia Movement Probe positioning (penumbra effect) (erroneously low SpO2) External light  RESPIRATORY SYSTEM Hypoxaemia: Causes: Low inspired oxygen Hypoventilation Diffusion impairment Ventilation/Perfusion (V/Q) mismatch Intra-cardiac shunt  RESPIRATORY SYSTEM Gas and inhalant agent monitoring: The inspired and expired oxygen can be analysed at the common gas outlet to evaluate for hypoxic gas mixtures Inhalant agent monitoring by infrared absorption spectroscopy, can be performed by the monitor to evaluate the inspired and end-tidal fractions of inhalant anaesthetic. Allows for accurate administration of inhalant anaesthetics Large animals (produce large amounts of methane): Methane absorbs infrared light too and may lead to erroneously high inhalant anaesthetic reading. Special filters must exist to be more specific for the inhalant agent and CO2, and avoid methane interference.  MECHANICAL VENTILATION Most commonly by positive pressure ventilation. Volume-controlled Pressure-controlled Other modalities.  TEMPERATURE Core temperature: at the pulmonary artery at end expiration pause. Can be approximated at deep oesophagus with a thermometer probe. Other locations for body temperature measurement: Rectal temperature Tympanic membrane (radiant infrared) Intranasal Axilla If peripheral temperature vs body core temperature difference is high = shock Animals with large body surface area : body mass ratio (smaller animals) = more heat loss and at higher risk of hypothermia In addition, during anaesthesia: Less metabolic rate for heat production Less muscle contraction Vasodilation (improves peripheral blood flow and dissipation of heat) Large areas of the body exposed to the environment (heat loss via irradiation and evaporation) Pyrexia and malignant hyperthermia can also develop Presence of heat moisture exchanger, low flow anaesthesia in a rebreathing system can also lead to hyperthermia (larger animals +++)  TEMPERATURE Hypothermia: Decreased body temperature by more than 1 standard deviation below normal mean core temperature for the species at rest. Dogs: < 37.8oC; severe < 34oC. Oesophageal temperature measurement is 0.4oC higher than rectal temperature (but influenced by environmental factors). Mechanisms of heat loss under anaesthesia: ↓ metabolic rate Fasting ↓ thermoregulatory response threshold is reduced No shivering (less heat production)  TEMPERATURE Heat loss process: 1. Redistribution phase: redistribution of heat from the core to the periphery. Due to vasodilation Loss of 1.5 oC within 1h Pre-warming can reduce core to periphery temperature difference = slows redistribution phase. 2. Linear phase: slower heat loss. Mechanisms: Radiation (40%) Convection (30%) Evaporation (25%) Conduction (5%) Passive insulation + active warming must be applied to avoid heat loss. 3. Plateau phase: core temperature plateau (equilibrium between heat loss and production). At 34oC: vasoconstriction may develop to reduce peripheral blood flow, reducing body core heat loss. Maintain good ambient temperature + good insulation + active warming + amino acids infusion?  TEMPERATURE Effects of hypothermia: CNS depression; CVS depression; Hypoventilation Low metabolic rate (↓10% per 1oC in core temperature): ↓ drug metabolism (overdose likely + prolonged recovery). ↓ Na+/K+ ATPase pump activity = cell oedema; cell death; hyperkalaemia; acidosis. Organoprotection (mainly CNS protection by ↓ metabolic rate for oxygen). ↑ Blood viscosity Hypocoagulation: splenic platelet sequestration. CNS activity: depression, therefore ↓ MAC by 5% per each ↓ 1oC of core temperature; this is due to CNS depression, and ↑ gas solubility in blood.  TEMPERATURE Myocardial effects: Slows conduction velocities (predisposes to arrhythmias) Decreases non-responsive to anticholinergic ECG: ST segment depression; T-wave inversion; R-R interval increased; QRS widening; “J” waves. Bradycardia; hypotension; lower cardiac output and organ perfusion SVR increases if 37.0 oC Cats can also develop hyperthermia on recovery (opioid-induced; the more pronounced is the hypothermia, the higher the body temperature on recovery)  NEUROMUSCULAR JUNCTION Useful when administering neuromuscular blocking drugs Monitor the neuromuscular function: Ensuring adequate paralysis and return of normal function Reduces risks of muscle weakness and airway obstruction on recovery Neuromuscular stimulation can be painful (do it only under anaesthesia) Ensure that the electrodes / subcutaneous needles are kept in place from induction of paralysis to recovery, to avoid erroneous interpretation Check details of monitoring in neuromuscular blockade lecture.  RENAL FUNCTION Important to monitor MAP; because if hypotension (