VENTILATOR MADE EASY BY DR.A AGLAN MD CRITICAL CARE DEPARTEMENT ALEXANDRIA UNIVERSITY CONTRIBUTING AUTHERS *** CONTENTS * Introduction - p Chapter 1* What is a ventilator? -p Chapter 2* The respiratory system -p Chapter 3* Ventilation -p Chapter 4* Patient – ventilator inter action p Chapter 5* Complications of invasive ventilation -p Chapter 6* Monitoring the patient on a ventilator -P Chapter 7* Ventilation of special cases p Chapter 8* Endo tracheal entubation -p Chapter 9* Drugs used during ventilation p Chapter 10* Care of ventilated patient -p Chapter 11* Nutrition of mechanically ventilated patient…………… P Chapter 12* In- hospital transport of mechanically ventilated paient Chapter WHAT IS A VENTILATOR? WHAT IS A VENTILATOR ** Definition; It is a machine designed to alter, transmit, and direct applied energy in a predetermined manner to augment or replace the patient s muscles in performing the work of breathing **Composition; *It is formed of parts:1- Power input : - a – Electricity 220 v or 110 v b – Gases O2 & air 3~ bar 2- Power transmission to down regulate electric and gases load to the control circuit 3-Controle circuits, It may be mechanical, pneumatic, fluid, electric, and or electronic ** All the above three parts are engineering problems 4- Control variables * The main function of the ventilator is to deliver air to the patient, and the physical characters of air which are changeable are called variables These are the flow, the volume, the time, the pressure, and the oxygen concentration (FiO2) * These variables are preset by the operator as value and shape depending on the mode and the type of the ventilator Pressure – Phase variable Limit or Target Cycle off Flow- Volume- Pressure- Time Baseline PEEP or Atmospheric Rising time Inspiratory pause Trigger Flow- Pressure- Time - Volume * The ventilator does not know the pattern of respiration, so it has been programmed to understand the phases of respiration which has been divided into phases as follow:- 1- Change from expiration to inspiration = triggering 2- Inspiration = limits or target 3- Change from inspiration to expiration = cycle off 4- Expiration = baseline * With each phase of the cycle any of the variables can be used (Time, Volume, Flow, or Pressure.) **Let us go and sea how the ventilator reacts and responds to the patient efforts 1- The patient starts to take inspiration by making change in the flow, pressure, or volume which is sensed by the demand valve of ventilator which opens whenever it reached the preset value * Sure each ventilator has its own demand valve system which responds to flow, pressure or volume *If the patient is paralyzed the ventilator will start inspiration automatically by time (60/RR) /min 2- Then after opening the demand valve air flows to the patient , but the machine asks you please how fast you need this flow? This means that you have to preset the flow ( peak flow ) or the rising time 3- Then the ventilator asks again please the flow to the patient developed pressure as a result of the resistance and compliance please would you set a limit to this pressure as an alarm or would put a maximum not to be exceeded this means you have to put the p limit or the p max 4- A good question comes from the ventilator; please this phase should be terminated (cycled) please can you set a time or a flow or a pressure or a volume a- You can inform (set) the ventilator please close the inspiratory limb after a set VT and keeps this VT in for some time ( inspiratory pause ) and then later open the expiratory valve, or open the expiratory valve immediately after the closure of the inspiratory limb ( no inspiratory pause ) ( volume targeted type as BENNET ) b- Please close the inspiratory limb after certain time (Ti), take a pause or not and then open the expiratory valve ( pressure targeted ,time cycled as ADULT STAR ) A question comes from the ventilator what about the VT ? I should answer that the VT will be adjusted via manipulating the target pressure, the flow ,the rising time ,and the Ti in addition to the parameters of the lung (compliance & resistance ) c- You have a pressure target which should not be exceeded please close the inspiratory limb after delivery of the preset VT, and then open the expiratory valve after the elapse of the Ti (DRAGER) What will happen when if? 1- The Ti is longer than the time for the preset VT? An inspiratory pause will be developed –The Ti is the same as that for the preset VT? No inspiratory pause will appear 3- The Ti is less than that of the preset VT? a volume less than the preset VT will be delivered and an alarm will signal So you have to adjust by either in creasing the Ti, or increasing the target pressure, or increasing the flow 5- The last question of the ventilator please, shall I allow all the VT to be exhaled totally and reach the atmospheric pressure or shall I keep some air inside (above the FRC) to produce a preset pressure above the atmospheric pressure at the end of expiration (PEEP) So you have to set the value of the PEEP or not ** From the phase variable items have emerged; A- The types of respiration; ** As we have mentioned before that the phase variable is formed of four phases , the trigger and the cycle phases which could be a patient or a machine function but the limit and the base phases are only a machine function Accordingly, we have divided the respiratory cycle of the ventilator into two types :1- Spontaneous 2- Mandatory 1-SPONTANEOUS CYCLE ** This means that the patient starts (trigger) and terminates (cycle off) the inspiration ** This means that the inspiratory time is that of the patient (neural time), which is determined by the patient and no rule for the machine Ti and accordingly no mismatching with the ventilator ** This type of respiration can be supported by the ventilator as in PSV where the triggering and cycling are of the patient but the limit is aided by the ventilator ** Trigger may be by use of pressure or flow sensor valve according to type of the ventilator used ** Termination of inspiration (cycle off) is determined by the device built in the ventilator and these may be: 1- Increase in expiratory flow 1-2 L/m above the inspiratory flow level 2- Increase in expiratory pressure 1-2 cmH2O above the inspiratory level ** What are the factors which determine the value of the VT.? ? * VT is determined by: 1- Patient inspiratory time 2- Pressure support of the ventilator 3- Lung compliance and resistance 4- Patient drive * So it is the pressure gradient developed between the negative pressure developed by the drive, inspiratory pump, and lung compliance of the patient and the pressure support developed by the ventilator ** Can I make any change in this VT?? * Sure yes, you can adjust VT by adjusting the pressure support in (PSV ) or (PEEP) IN CPAP ,and the difference between the high PEEP and low PEEP in BiPAP * 2- MANDATORY CYCLE ** There are two types: 1- Triggering and cycling are done by the ventilator as in paralyzed patient (CMV) 2- The patient triggers but the ventilator terminates (cycle off) the inspiration, so it is a share between both the patient and the ventilator (ACV) * How does the ventilator end the cycle? This is built in device in the machine which may be; 1- Volume, when a preset VT is achieved 2- Flow, when the flow drops to 5L/ m or the flow drops to 25% of the peak flow 3- Time, when the machine Ti (preset Ti) is achieved * It is clear that the ventilator does not sense the start of the patient expiration and even is not sensitive to the termination of the patient inspiration This means that the neural Ti will not match the machine Ti and so mismatch will occur leading to a lot of problems *What about the respiratory rate? * Sure it is that of the patient which is affected by the set flow, set VT, and the ventilator Ti * What about the VT ? * In volume targeted pressure limit, it is the preset VT * In pressure targeted, volume controlled, time cycled it is the preset VT *In pressure targeted, time cycled, I/E cycled it will depend on the target pressure, flow, Ti, I/E, and patient parameters Ventilator Breaths And Phase Variables Type Of Ventilation Trigger Limit Cycle Mandatory Assisted Supported Spontaneous Machine Patient Patient Patient Machine Machine Machine Patient Machine Machine Patient Patient B- The types of the respiratory cycle (types of ventilator) ** Positive pressure (which supply air with positive pressure through the ETT.), and negative pressure ventilator (which produces negative pressure around the chest wall ) **Ventilators have been divided into two types according to the target undependable fixed variable:2- Pressure targeted 1- Volume targeted ** This division has been built on the relation between the VT, PL., and the compliance which is controlled by the flowing equation;C = VT / PL * It is clear from this equation that you will adjust the variables where the parameter C is fixed, so in one ventilator you will set and change the VT and accordingly the P will change according to the C (volume targeted), and I the other one you set or change the P( P max) and accordingly the VT will be determined by the C( pressure targeted) ** Volume targeted ventilators delivers VT irrespective to the state of C or the degree of change in the PL So when the C is bad the PL, and accordingly the PIP will be high, but when the C is good the PL, and PIP will not be increased much as in the following diagram * So in cases of bade (low) C when the preset VT is delivered the PL will increase too much and this may expose the alveoli to over distension and volutrauma Also, if the patient developed Pneumothorax, the VT will be delivered totally leading to more increase in the pleural pressure pressing on the cardiac fossa to produce cardiac tamponade The patient will die from C.V collapse The monitor in such type will be the PL and the homodynamic Such ventilators are harmful to infants and children * **PRESSURE TARGETED VENTILATORS:The maximum pressure is preset; this sealing pressure is not exceeded by any mean The tidal volume for sure will be determined by the following:1 –the compliance 2- the preset pressure 3- the flow – the inspiratory time So increase or decrease of any of the above will be associated with increase or decrease of the VT as is demonstrated by the following diagram * In case of Pneumothorax with the same setting of flow, pressure, and time the VT will decrease and the patient will develop hypoxia So the monitor in such type will be the change in the VT and blood gases (O2 & CO2) Such ventilators are safer regarding volutrauma In certain ventilators as ADULT STAR the VT is not preset but it is the result of the empirical values of the preset variables, FLOW, PR., and Ti which match the compliance of the patient So adjustment of these variables is needed to reach to the desired VT In other ventilators as DRAGER the VT is preset so called volume controlled, where the inspiratory limb of the ventilator is closed after delivery of the preset VT and the expiratory limb is opened after the lapse of the Ti This means that you will face one of three situations:1- The VT is delivered in a time less than Ti so the difference will be inspiratory pause 2- The VT is delivered in a time equal to the Ti so there will be no inspiratory pause In adults it may be given as (1) bolus of 100 to 250 ml every – h (2) continuous infusion starting at 25 – 30 ml/h to be increased by 10 – 25 ml/h every to has tolerated ( gastric residual volume < 150 ml) until the caloric requirement is delivered ( usually met within two days) Gastric residual volume should be monitored every 4h, before giving the next bolus When gastric residual volume is > 150 ml, feeding should be with hold for h, and then resumed Failure to give gastric feeding should lead to shift to small bowel feeding Feeding formula should not be diluted because the formula osmolality is typically 300 to 600 mosm /kg of water, and this rarely causes diarrhea CONCLUSIONS **Nutritional support is an important aspect of the treatment of the critically ill, hyper catabolic patient **It is essential to start enteral feeding as soon as the patient is stabilized **Parenteral feeding should be started only if enteral feeding is poorly tolerated, and not simply as an additive to it **Adding special nutrients to enteral nutrition does not appear to decrease mortality, with the possible exception of adding glutamine in burns patients **Adding glutamine to parenteral nutrition is beneficial Nutritional support can improve clinical outcomes in certain disease states **When adequate nutrition cannot be supplied, morbidity increases REFERENCES Dudrick SJ, Wilmore DW, Vars HM, Rhoads JE Long term total parenteral nutrition with growth development, and positive nitrogen balance Surgery 1968; 64: 134-142 Alexander J Immunoenhancement via enteral nutrition Arch Surg 1993; 128:1242-1245 Deitch E Gut failure: Its role in multiple organ failure In: Multiple Organ Failure Deitch E (ed): New York, Thieme Medical Publisher 1990: 40-60 Lavery G The metabolic and nutritional response to critical illness In: Oxford textbook of critical care Webb AR, Shapiro MJ, Singer M, Suter PM (eds.) Oxford, Oxford University Press 1999: 383386 Gabe SM, Grimble GK Patophysiology of nutritional failure In: Oxford textbook of critical care Webb AR, Shapiro MJ, Singer M, Suter PM (eds.) Oxford, Oxford University Press 1999: 386-390 Dark DS, Pingelton SK Nutrition and nutritional support in critically ill patients J Int Care Med 1993; 8: 16-33 Giner M, Laviano A, Meguid MM, Gleason JR In 1995 a corrolation between malnutrition and poor outcomes in critically ill patients still exists Nutrition 1996; 12: 23-29 Heyland DK Nutritional support in the critically ill patient: A critical review of the evidence Crit Care Clin 1998; 14: 423-440 Heyland DK, Cook DJ, Schoenfeld PS, Frietag A, Varon J, Wood G The effect of acidified enteral feeds on gastric colonization in the critically ill patient: Results of a multicenter randomized trial Crit Care Med 1999; 27: 23992406 10 Mentec H, Dupont H, Bocchetti M, Cani P, Ponche F, Bleichner G Upper digestive intolerance during enteral nutrition in critically ill patients: Frequency, risk factors and complications Crit Care Med 2001; 29: 1955-1961 11 Heyland DK, MacDonald S, Keefe L, Drover JW Total parenteral nutrition in the critically ill patient: A metaanalysis JAMA 1998; 280: 2013-2019 12 Heyland DK, Dhaliwal R, Drover JW, Gramlich L, Dodek P Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients JPEN 2003; 27: 355373 * How to plan for nutritional support? * You have to discuss three factors which are; 1- Current nutritional state 2- Anticipated duration of inadequate nutrition 3- Degree of stress response 1- Current of nutritional state * It includes the following; 1- History of illness as vomiting, diarrhea, weight loss, and so on 2- Physical examination 3- Body mass index (BMI) where a value of 18 means significant malnutrition 4- Upper arm anthropometry, where mid arm circumference and triceps skin fold thickness, reveal information about lean body mass and fat reserves A value below 5th percentile is consistent with loss of about 30% of the lean body mass 5- Lab Values as; 1- Serum * albumin * pre albumin * transferrin * retinol- binding protein * IGF 2- 24 h nitrogen in urine, provides an indirect measure of the severity of stress 3- Creatinine height index (CHI) is the ratio of measured Creatinine excreted to the expected of control subject matched with age, sex, and ideal body weight Values < 85% indicates moderate loss of lean body mass, but value < 60% signifies severe loss 2- Anticipated duration of inadequate nutrition * When to start nutrition depends on the nutritional state and the severity of illness * Patients with moderate malnutrition and moderate stress can be provided with nutrition within to days * Critically ill patients should be given nutrition within 48 to 72 h (immediately after stabilization) * Enteral feeding is the best and physiological one, but relative or absolute contra indications can appear as, severe diarrhea, ischemic bowel, ileus, high NGT out put, pancreatitis, hemodynamic unstability, or use of Alfa agonist * TPN should be started to improve metabolic state, electrolyte balance, micro and macro nutrients, acid base status, drug delivery, and ensure nutrient delivery till enteral feeding is allowed 3- Degree of stress * It depends on the severity of illness and the score of morbidity as trauma, burns, and infection * Evaluation of energy expenditure (EE) which can be done as follow; 1- Direct calorimeter from the heat loss (it is a lab method) 2- QT & A-V O2 content difference, where the O2 uptake is measured from the equation (QT mi/min x (arterial O2 content – venous O2 content) x 100) Since consumption of L O2 for mixed diet will produce 4.8 K cal The EE = O2 uptake / X 4.8 3- From empirical formulas; 1-Harris & Benedict equation * Men BMR = 665.0 + 13.7w + X h – 6.78 A * Women BMR = 655.0 + 9.56 W + 1.85 h – 4.68 A W = Weight H = Height A = Age years * EE = BMR - 10% for starvation = BMR + 10% for elective surgery = BMR + 10% for trauma = BMR + 30% for sepsis = BMR + 50% for burns 2- B.W X 25 to 40 Kcal according to the severity of illness 3- N loss/ day x 100 to 200 Kcal according to the severity of illness *What are the nutritional elements? * These nutritional elements are; 1- Carbohydrates- glucose 2- Fats 3- Proteins 4- Water 5- Minerals 6- Trace elements 7- Vitamins ** GLUCOSE * Glucose has one of metabolic fates; 1- Oxidation for energy 2- Forms the serum pool 3- Conversion to glycogen 4- Conversion to fat * g glucose consumes 0.8 L O2 to produce 0.8 L CO2 and give 4.14 Kcal * The minimal dose is 2.5 mg/ kg /min to give sufficient energy, to brain cells, blood cells, and fibroblasts, to prevent excessive lipolysis and ketosis, and to avoid starvation * The maximum dose is 7.5 mg/kg/ where glucose toxicity and over feeding will occur due to the transformation of glucose to fat in the liver cells to manifest as; 1- Over production of CO2 due the high RQ (= 8) for the conversion of glucose to fat, and this may form a high preload on the respiratory system especially for those with limited minute volume as COPD patients 2- Increase in the core temperature 3- Liver steatosis due to intra cellular fat deposition with increase in liver enzymes and intrahepatic cholestasis * Glucose should be given slowly as mentioned to avoid its loss in urine and induction of diuresis * It should be given in large central vein to minimize thrombophlebitis because it is usually given with high concentration * Infusion of glucose is usually associated with both hyper glycemia and hyper insulinemia which inhibit lipolysis depriving the body from its internal source of essential fatty acids, so you have to supply it as a complementary source of energy with glucose ( 50% each) or every other day (when glucose supply is below the toxic level and satisfy the energy requirements) * With IDDM (type I) you have to add 1U soluble insulin for each 20 g glucose * With NIDDM (type II) you have to add 1U soluble insulin for each 3- g glucose * For basal insulin start with 1U soluble insulin /h for NIDDM and 0.5 U soluble insulin /h for IDDM and adjust by adding 0.3 U for each increase of RBS 60 mg% * 1U soluble insulin is considered for metabolizing 10 to 15 g oral carbohydrates * Critically ill patients might have high blood glucose level due to low insulin, increase in the insulin counter regulatory hormones, increase in the insulin resistance due the effect of cytokines, and increase gluconeogenesis (which is suppressed by DW in the non stressed person but with blood glucose level of 600mg% in the critically ill patient) * Tight glycemic control (RBS at 110 mg %) is important in critically ill to reduce morbidity and mortality * With head trauma it is important to control glucose at 100 mg % to guard against the lethal effect of the H paradox (high blood glucose lead to intra cellular acidosis) * Hypernatremia should not be corrected with DW due to the fact that insulin resistance is present in such condition and adding glucose might worsen the osmolality state ** PROTEINS * Protein is present in one of three forms; 1- Structural 2- Functional 3- Amino acid pool * I.V protein is incorporated in one of these forms or oxidized to give glucose and urea * In critically ill patients there is an increase in the proteolysis- negative N balanceto; 1- Supply energy through gluconeogenesis 2- Supply BCAA for tissue repair 3- Supply good substrates for acute phase protein 4- Increase the immune mechanisms through release of arginine, glutamine and formation of acute phase proteins * Protein needs for critically ill goes up to 1.5 g/kg /day * When protein intake exceeds 1.7 g/kg/ day urea genesis increases rather than protein synthesis * Nitrogen is lost from skeletal muscles, liver, kidney, gut, and lung but is not lost from the brain, nervous tissue, and the extracellular matrix in critically ill patients * The minimal daily requirements of N is 60 mg/kg to maintain N balance at zero * On fasting N loss will be 3.6 g /day * In critically ill patients as in burns the negative N balance may go up to 27 g / day * Decrease in energy supply will increase N loss due to the increase in the gluconeogenesis, so it is mandatory to give full caloric supply from carbohydrates and fat to save protein * Enteral feeding is more effective in controlling N balance * Increase in N requirement is associated with increase in energy expenditure * g urea = 1g N = 6.25 g protein = 30 g flesh * It is easy to calculate the daily N loss from 24 h urine collection and measuring the total content of urea * 1g protein needs 0.9 L O2 to give 0.7 L CO2 to give 4.4 Kcal * Branched chain amino acids (BCAA) Valine, Leucine, and Isoleucine are among the nine essential AA in human being They account for 35% of the essential AA and 14% of the total AA in the skeletal muscles * BCAA are very important because they; 1- Are metabolized by the skeletal muscles and not by the kidney, so they not contribute directly to urea production 2- Compete with the aromatic AA for their entry to the brain (they have the same receptors), so they decrease its entry to the brain to decrease hepatic encephalopathy 3- Share gluconeogenesis 4- Share the formation of the acute phase protein 5- Share the synthesis of glutamine 6- Improve protein formation * Glutamine; - It is a non essential AA - It forms 60% of the intracellular pool of the AA - It is synthesized from glutamate, serine, aspartate, and to a lesser extent from BCAA - Decreases in critically ill by 50% - Its formation is increased in the critically ill by the skeletal muscles from the BCAA - It is very important for the rapidly proliferating cells, endothelial cella to guard against injury, lymphocytes to increase immunity, gut mucosa to increase digestion, absorption, and decrease translocation and protein loss, and fibroblast for repair - It is very important to the kidney to produce NH3 to combat H+ and increases its secretory capacity of the acid load * Arginine; - ** LIPIDS * In critically ill patients there is an increase in lipolysis in the fat depot and skeletal muscles, with an increase in the serum glycerol level due to local defect of glycerol kinase, but the serum level of FFA does not increase due to the fact that it is reesterified locally So glycerol level is a good monitor to the degree of lipolysis * High glucose infusion and high insulin level suppress lipolysis to deprive the body from its essential FA that is why it should be supplied to the patient daily or every other day * FA as long chain one (linoleic acid) should be given in a dose of to g/ kg /day * The infusion rate should not exceed mg /kg / * It should not be given to patients with TG > 400 mg% * It is acted upon by PLA to produce Arachidonic acids and then the other by product mediators which increases shunt and sepsis reactions, so it is better not to be given in such cases * Long chain FA as linoleic acid is important for lipid formation in the body * Medium chain FA as oleic a, palmitic a linolenic a and stearic a are used for energy production, not stored, not infiltrating, but ketogenic * Intralipid has LCFA linoleic acid 54%, and MCFA as oleic acid 26%, palmitic acid 9%, linolenic acid 8%, and stearic acid 3% * 1g fat needs L O2 to produce 1.4 L CO2 and give 9.3 Kcal * What are the benefits of lipid infusion? 1- Supply essential FA 2- Decrease glucose toxicity 3- Decrease infused volume 4- Does not produce phlebitis * What are the complications of lipid infusion? 1- It inhibits the R.E.S 2- It increases the infection rate 3- It increases the production of PG ** WATER * Daily requirement for adult is 100 ml /kg or ml / Kcal, but for children and infants are 150 ml /kg or 1.5 ml /Kcal * ** MINERALS * Daily requirements are; *Na meq / kg * K 1meq / kg * Mg 0.5 meq /kg I.V or mg /kg orally * Ca 0.5 meq /kg I.V or 15 mg /kg orally * Phosphorus 0.5 meq /kg I.V or 15 mg /kg orally * Adjustment of these minerals should rely on the balance between intake output and their blood level * With R F, k, Mg, and Phosphorus accumulate and dietary restriction may be warranted **TRACE ELEMENTS * The commonest trace elements are iron, iodine, cobalt, zinc, copper, chromium, manganese, and selenium * These trace elements should be supplied as recommended daily allowance(RDA) ** VITAMINES * Both fat and water soluble vitamins should be supplied as RDA ** Nutrition for specific disease states 1** Systemic inflammatory response syndrome (SIRS) * Early enteral nutrition is important * Immune nutrition with arginine, omega FA, and glutamine have been associated with decrease in, infection, hospital stay, and mortality *Full TPN and PN should be provided to restore N balance * You should supply at least 200 mg /kg as N or 1.4 g protein / kg /day * If EE IS measured (indirect calorimeter) provide energy (carbohydrate, lipid and protein) at 1.33 times REE with the non protein calories given aw 50% carbohydrates and 50% fat, with a calorie: N ratio of 150 Kcal/ g N * If REE is not measured, provide 2800 Kcal / day or 40 Kcal /kg /day, with a calorie: N ratio of 150 Kcal / g N 2** Acute pancreatitis; * Certain important facts should be considered and these are : 1- Oral feeding is difficult and prohibited due to; * Abdominal pain * Nausea * Vomiting *Gastric atony * Paralytic ileus *Partial duodenal obstruction due to pancreatic enlargement * Decrease pancreatic enzymes * Decrease absorption * Increase protein loss as a result of inflammation of peritoneal and retro peritoneal surfaces, diarrhea, or fistula 2- Increase in EE by 50 % to 150 % 3- Carbohydrate metabolism is altered leading to; * Hyperglycaemia due to damage to B cells * Decrease insulin secretion * Increase insulin resistance * Increase gluconeogenesis 4- Fat metabolism is altered leading to; * Increase lipolysis * Increase lipid oxidation * Hyper lipidemia and hyper TG due to decreased plasma clearance 5- Protein metabolism shows; * Increase catabolism * Increase urea formation * Increase N loss (20 to 40 g/day) 6- Micronutrients and vitamins decrease due to decrease intake * Haw to adopt enteral feeding? **1- Enteral nutrition should be the preferred rout where TPN and pancreatic Rest (no enteral feeding) proved to be of no benefit, but may be harmful ** 2- Early TPN may be started for those who can not tolerate enteral one, but enteral feeding should be resumed as early as possible 3** Acute renal failure * Such patients should be fed via the enteral rout * Hyper catabolism, increase nutrient loss, and or increase nutrient demand through dialysis mandate increase in the quantities of nutrients * Patients not on dialysis should be given; * Protein 1.0 g/ kg /day for non hyper catabolic cases * Protein 1.2 to 1.5 g /kg /day for poly trauma, infection, and burn cases * Caloric intake as carbohydrates and fat at 25 to 40 Kcal /kg /day * Oliguric and anuric patients should receive smaller volumes of fluids and electrolytes ( K, Kg, and phosphorus which are retained) * Patients on dialysis should be given; * Protein 1.2 to 1.5 g/kg /day to compensate for hyper catabolism and loss through dialysis (haemo or peritoneal dialysis) * With peritoneal dialysis you should consider the absorbed glucose from the dialysate for the caloric calculation 4** Liver disease *When there is no encephalopathy; * Protein intake should be to 1.3 g/kg/day * Fluid restriction to decrease ascites and oedema * Electrolytes adjustment for hypo kalemia, magnesemia, and low zinc * Caloric intake adjustment at 25 to 40 Kcal /kg /day * With encephalopathy; * Protein intake should be at to 1.3 g/kg/day, but with high BCAA, low aromatic AA , and low sulphur- containing AA (this formula does not improve outcome but improves mental status * Keep an eye on RBS to guard against hypoglycemia * Adjust fluid according intake output and body water contents * No trials of enteral nutrition in fulminant liver failure (viral or drug induced) have been conducted 5** Respiratory system * In critically ill patients there is increase in EE, with increase O2 demand and CO2 production which means increase in the respiratory work load which may lead to relative respiratory failure * Increase in glucose feeding to the toxic level 7.5 mg/kg/min, will increase fat formation with RQ= which mean higher production of CO2, high fever, and liver steatosis (increase liver enzymes and cholestatic jaundice) * There is a linear relation between body weight and diaphragm weight, which mean loss of body weight in critically ill is associated with loss of diaphragm weight * Protein loss is common due to malnutrition, hyper catabolism and drug induced (muscle relaxants, steroids, and aminoglycosides) So it is important to give high protein at 1.5 g/kg/day in addition to antioxidants, vitamins, minerals And trace elements *What are the effects of nutrition on weaning? * It has two contradictory effects; a- Short terms effect with increase in, CO2 production, ventilatory drive, and work load b- Long term effects with increase in serum albumin and decrease in lung water which improve respiratory function ( muscle mass, surfactant, lung parenchyma, and immunology ) * It is important to adjust nutrition to decrease short term effects and increase long term effects to make weaning easy * Enteral feeding may produce some problems to the ventilated patient as mal positioning, aspiration, sinusitis, and otitis media 6** Malnutrition; *There is a loss of the body cell mass (BCM) in the ratio of parts BCM to one part fat *N intake should be given in the range of 300 to 350 mg/kg/day *The average REE is usually 26 Kcal /kg /day * Energy supply = EE + 25% to 50% * If EE is measured, provide energy at 1.25 x REE for bed ridden, and 1.5 x REE for ambulatory, with a calorie : N ratio of 100Kcal/g N * If EE is not measured, provide 200 Kcal/day or 32 Kcal /kg /day for bed ridden and 2400Kcal/day or 39 Kcal /kg /day for ambulatory patients, with a calorie : N ratio of 100 Kcal/g N, these formulas will provide 20 Gn /day for the bed ridden and 24 g N /day for the ambulatory * With sepsis or trauma, malnourished patients should receive an increase in calories but with calorie to N ratio of 100 Kcal / g N Chapter 12 * IN - HOSPITAL TRANSPORT OF MECHANICALLY VENTILATED PATIENT * PROCEDURE: Transportation of a mechanically ventilated patient for diagnostic or therapeutic procedures *DESCRIPTION/DEFINITION: Transportation of mechanically ventilated patients for diagnostic or therapeutic procedures is always associated with a degree of risk.(1-9) Every attempt should be made to assure that monitoring, ventilation, oxygenation, and patient care remain constant during movement Patient transport includes preparation, movement to and from, and time spent at destination * SETTINGS: This guideline is intended for the critical care and acute care inpatient setting * INDICATIONS: Transportation of mechanically ventilated patients should only be undertaken following a careful evaluation of the risk-benefit ratio *CONTRAINDICATIONS: Transportation of the mechanically ventilated patient should not be undertaken until a complete analysis of potential risks and benefits has been accomplished * Contraindications include * Inability to provide adequate oxygenation and ventilation during transport either by manual ventilation, portable ventilator, or standard intensive care unit ventilator,(1,10-12) * Inability to maintain acceptable haemodynamic performance during transport,(13-15) * Inability to adequately monitor patient cardiopulmonary status during transport,(14) * Inability to maintain airway control during transport * Transport should not be undertaken unless all the necessary members of the transport team are present * HAZARDS & COMPLICATIONS: Hazards and complications of transport include the following: *Hyperventilation during manual ventilation may cause respiratory alkalosis, cardiac dysrhythmias, and hypotension.(1,10,11) * Loss of PEEP/CPAP may result in hypoxemia or shock.(16,17) * Position changes may result in hypotension, hypercarbia, and hypoxemia.(14) * Tachycardia and other dysrhythmias have been associated with transport.(13-15) * Equipment failure can result in inaccurate data or loss of monitoring capabilities.(8,9) * Inadvertent disconnection of intravenous access for pharmacologic agents may result in haemodynamic instability.(8,9,13) *Movement may cause disconnection from ventilatory support and respiratory compromise.(16,18) * Movement may result in accidental extubation.(13,19) * Movement may result in accidental removal of vascular access.(3-5,8,9) * Loss of oxygen supply may lead to hypoxemia * Ventilator-associated pneumonia has been associated with transport.(20) * LIMITATIONS OF METHOD: The literature suggests that nearly two thirds of all transports for diagnostic studies fail to yield results that affect patient care.(8,9) *ASSESSMENT OF NEED: The necessity and safety for transport should be assessed by the multidisciplinary team of health care providers, eg, respiratory therapist, physician, nurse The risks of transport should be weighed against the potential benefits from the diagnostic or therapeutic procedure to be performed * ASSESSMENT OF OUTCOME: The safe arrival of the mechanically ventilated patient at his/ her destination is the indicator of a favorable outcome * RESOURCES: *** Equipment * Emergency airway management supplies should be available and checked for operation before transport * Portable oxygen source of adequate volume * A self-inflating bag and mask of appropriate size * Transport ventilators have been shown to provide more constant ventilation than manual ventilation in some instances If a transport ventilator is used, it should:(1,10-12,21,22) * have sufficient portable power supply for the duration of transport;(23) * have independent control of tidal volume and respiratory frequency;(16) * be able to provide full ventilatory support as in assist-control or intermittent mechanical ventilation (not necessarily both); * deliver a constant volume in the face of changing pulmonary impedance; * monitor airway pressure; * provide a disconnect alarm; * be capable of providing PEEP; * provide an FIO2 of 1.0 * A pulse oximeter is desirable *Appropriate pharmacologic agents should be readily available * Portable monitor should display ECG and heart rate and provide at least one channel for vascular pressure measurement * An appropriate hygroscopic condenser humidifier should be used to provide humidification during transport * Stethoscope * Hand-held spirometer for tidal volume measurement * Personnel: All mechanically ventilated patients should be accompanied by a registered nurse and a respiratory therapist during the entire transport * At least one team member must be proficient in managing the airway in the event of accidental extubation * At least one team member should be proficient in operating and troubleshooting all of the equipment described in Section 10.1 * MONITORING: Monitoring provided during transport should be similar to that during stationary care * Electrocardiograph should be continuously monitored for heart rate and dysrhythmias * Blood pressure should be monitored continuously if invasive lines are present In the absence of invasive monitoring, blood pressure should be measured intermittently via sphygmomanometer * Respiratory rate should be monitored intermittently * Airway pressures should be monitored if a transport ventilator is used.(24) * Tidal volume should be monitored intermittently to assure appropriate ventilation.(25) * Continuous pulse oximetry is appropriate during transport of all mechanically ventilated patients * Breath sounds should be monitored intermittently * FREQUENCY: Patients should be transported only when indications are present as described above * INFECTION CONTROL: * Universal Precautions should be observed.(26) * All equipment should be disinfected between patients * Centers for Disease Control and Prevention recommendations for control of exposure to tuberculosis and droplet nuclei are to be implemented when patient is known or suspected to be immuno suppressed, is known to have tuberculosis, or has other risk factors for the disease.(27) References Braman SS, Dunn SM, Amico CA, Millman RP Complications of intrahospital transport in critically ill patients Ann Intern Med 1987;107(4):469-473 Edlin S Physiological changes during transport of the critically ill Intensive Care World 1989;6:131 Smith I, Fleming S, Cernaianu A Mishaps during transport from the intensive care unit Crit Care Med 1990;18(3):278-281 Insel J, Weissman C, Kemper M, Askanazi J, Hyman AI Cardiovascular changes during transport of critically ill and postoperative patients Crit Care Med 1986;14(6):539-542 Ehrenwerth J, Sorbo S, Hackel A Transport of critically ill adults Crit Care Med 1986;14(6):543547 Andrews PJ, Piper IR, Dearden NM, Miller JD Secondary insults during intrahospital transport of head-injured patients Lancet 1990;335(8685):327-330 Gentleman D, Jennett B Audit of transfer of unconscious head-injured patients to a neurosurgical unit Lancet 1990;335(8685):330-334 Indeck M, Peterson S, Smith J, Brotman S Risk, cost, and benefit of transporting ICU patients for special studies J Trauma 1988;28(7):1020-1025 Hurst JM, Davis K Jr, Johnson DJ, Branson RD, Campbell RS, Branson PS Cost and complications during in-hospital transport of critically ill patients: a prospective cohort study J Trauma 1992;33(4):582-585 10 Hurst JM, Davis K Jr, Branson RD, Johannigman JA Comparison of blood gases during transport using two methods of ventilatory support J Trauma 1989;29(12):1637-1640 11 Gervais HW, Eberle B, Konietzke D, Hennes HJ, Dick W Comparison of blood gases of ventilated patients during transport Crit Care Med 1987;15(8):761-763 12 Weg JG, Haas CF Safe intrahospital transport of critically ill ventilator-dependent patients Chest 1989;96(3):631-635 13 Taylor JO, Chulay JD, Landers CF, Hood WB Jr, Abelman WH Monitoring high-risk cardiac patients during transportation in hospital Lancet 1970;2(7685):1205-1208 14 Waddell G Movement of critically ill patients within hospital Br Med J 1975;2(5968):417-419 15 Rutherford WF, Fisher CJ Risks associated with inhouse transportation of the critically ill (abstract) Clin Res 1986;34:414 16 Branson RD Intrahospital transport of critically ill, mechanically ventilated patients Respir Care 1992;37(7):775-795 17 Komdeur R, van der Werf TS, Ligtenberg JJ, Tulleken JE, Zijlstra JG [Hemodynamic and ventilatory complications of mechanical ventilation with high intrinsic positive end-expiratory pressure.] Ned Tijdschr Geneeskd 2000;144(30):1445-1450 article in Dutch 18 Johannigman JA, Branson RD, Campbell R, Hurst JM Laboratory and clinical evaluation of the max transport ventilator Respir Care 1990;35(10):952-959 19 Christie JM, Dethlefsen M, Cane RD Unplanned endotracheal extubation in the intensive care unit J Clin Anesth 1996;8(4):289-293 20 Kollef MH, Von Harz B, Prentice D, Shapiro SD, Silver P, St John R, Trovillion E Patient transport from intensive care increases the risk of developing ventilator-associated pneumonia Chest 1997;112(3):765-773 21 Dockery WK, Futterman C, Keller SR, Sheridan MJ, Akl BF A comparison of manual and mechanical ventilation during pediatric transport Crit Care Med 1999;27(4):802-806 22 Tobias JD, Lynch A, Garrett J Alterations of end-tidal carbon dioxide during the intrahospital transport of children Pediatr Emerg Care 1996;12(4):249-251 23 Barton AC, Tuttle-Newhall JE, Szalados JE Portable power supply for continuous mechanical ventilation during intrahospital transport of critically ill patients with ARDS Chest 1997;112(2):560-563 24 Miyoshi E, Fujino Y, Mashimo T, Nishimura M Performance of transport ventilator with patienttriggered ventilation Chest 2000;118(4):1109-1115 25 McGough EK, Banner MJ, Melker RJ Variations in tidal volume with portable transport ventilators Respir Care 1992;37(3):233-239 26 Update: Universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other blood-borne pathogens in health-care settings MMWR 1988;37(24):377-382,387-388 27 Dooley SW Jr, Castro KG, Hutton MD, Mullan RJ, Polder JA, Snider DE Jr Guidelines for preventing the transmission of tuberculosis in health-care settings, with special focus on HIVrelated issues MMWR Recomm Rep 1990;39(RR-17):1-29 ... mismatching with the ventilator ** This type of respiration can be supported by the ventilator as in PSV where the triggering and cycling are of the patient but the limit is aided by the ventilator **... done by the ventilator as in paralyzed patient (CMV) 2- The patient triggers but the ventilator terminates (cycle off) the inspiration, so it is a share between both the patient and the ventilator. .. of ventilator) ** Positive pressure (which supply air with positive pressure through the ETT.), and negative pressure ventilator (which produces negative pressure around the chest wall ) **Ventilators