Transcript RT 230
RT 230 Unit AIndication, Setup and Monitoring of CMV INDICATIONS FOR CMV Apnea Acute ventilatory failure: A PCO2 of more than 50mmHg with a pH of less than 7.25 Impending acute ventilatory failure Based on lab data and clinical findings indicating that pt is progressing towards ventilatory failure Quick tip: acute hypercapnic failure ph drops 0.8 for every 10mm hg rise in co2 chronic hupercapnic ph drops 0.03 for every 10 mmhg rise in co2 Clinical problems often resulting in impending ventilatory failure Pulmonary abnormalities RDS=Respiratory Distress Syndrome Pneumonia Pulmonary emboli Mechanical ability of lung to move air=muscle fatigue Ventilatory muscle fatigue Chest injury Thoracic abnormalities=scoliosis, kyphoscoliosis Neurologic disease=GB, MG Pleural disease=pleurasy Clinical evaluation Vital signs: Pulse and BP increase Ventilatory parameters VT decreases RR increases Accessory muscle use increases Paradoxical breathing (abdomen out, rib cage in) Retractions may be noted Development of impending acute vent failure may demonstrate Progressive muscle weakness in pt with Neurologic disease Increasing fatigue ABGs demonstrating a trend toward failure 9am 10am pH PCO2 HCO3 PO2 11am 7.58 22 21 60 12pm 7.53 28 22 55 1pm 7.46 35 23 50 7.38 42 24 43 7.35 48 24 40 Non-responsive hypoxemia PaO2 less than 50% on an FIO2 greater than 50% PEEP is indicated REFRACTORY HYPOXEMIA PHYSIOLOGIC EFFECTS OF POSITIVE PRESSURE VENTILATION Increased mean intrathoracic pressure Decreased venous return Thoracic pump is eliminated*** Pressure gradient of flow to right side of heart is decreased Right ventricular filling is impaired Give fluid Decreased cardiac output Caused by decreased venous return Give drugs and fluid Monitor I and O. Normal urine output 1000-1500 cc/24 hours THORACIC PUMP The "thoracic pump" is the thoracic cavity, the diaphragm, the lungs, and the heart. The diaphragm moves down, pressure in the cavity decreases and venous blood rushes through the vena cava via the right heart into the lungs. Pulmonary blood vessels expand dramatically, filling with blood, air and blood meeting across the very thin alveolar surface. The deeper the inhalation, the more negative the pressure, the more blood flows, and the fuller the lungs become. THORACIC PUMP As the diaphragm moves up the pressure in the thoracic cavity reverses. Pulmonary blood vessels shrink ejecting an equal volume of blood out of the pulmonary veins into the left heart. The left heart raises the pressure and checks and regulates the flow. The more complete the exhalation, the more positive the pressure becomes and the more blood is ejected from the lungs. Decrease exhalation, more pressure in cavity decrease CO EFFECTS OF PPV CONT. Increased intracranial pressure Blood pools in periphery and cranium because of decreased venous return Increased volume of blood in cranium increases intracranial pressure Decreased urinary output PPV could cause 30-50% decrease renal output Decreased CO results in decreased renal blood flow Alters filtration pressures and diminishes urine formation Decreased venous return and decreased atrial pressure are interpreted as a decrease in overall blood volume ADH is increased and urine formation is decreased ADH=VASOPRESSIN Roughly 60% of the mass of the body is water, and despite wide variation in the amount of water taken in each day, body water content remains incredibly stable. Such precise control of body water and solute concentrations is a function of several hormones acting on both the kidneys and vascular system, but there is no doubt that antidiuretic hormone is a key player in this process. Antidiuretic hormone, also known commonly as arginine vasopressin The single most important effect of antidiuretic hormone is to conserve body water by reducing the loss of water in urine. A diuretic is an agent that increases the rate of urine formation. high concentrations of antidiuretic hormone cause widespread constriction of arterioles, which leads to increased arterial pressure. Retention of fluids will cause EDEMA EFFECTS OF PPV CONT. Decreased work of breathing Force to ventilate is provided by the ventilator Increased deadspace ventilation Positive pressure distends conducting airways & inhibits venous return The portion of VT that is deadspace increases Greater percentage of ventilation goes to apices Increased intrapulmonary shunt Ventilation to gravity dependent areas is decreased Perfusion to gravity dependent areas increase Shunt fraction increases from 2-5% to 10% A pulmonary shunt is a physiological condition which results when the alveoli of the lung are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region. In other words, the ventilation/perfusion ratio (the ratio of air reaching the alveoli to blood perfusing them) is zero. A pulmonary shunt often occurs when the alveoli fill with fluid, causing parts of the lung to be unventilated although they are still perfused. Intrapulmonary shunting is the main cause of hypoxemia (inadequate blood oxygen) in pulmonary edema and conditions such as pneumonia in which the lungs become consolidated. The shunt fraction is the percentage of blood put out by the heart that is not completely oxygenated. A small degree of shunt is normal and may be described as 'physiological shunt'. In a normal healthy person, the physiological shunt is rarely over 4%; in pathological conditions such as pulmonary contusion, the shunt fraction is significantly greater and even breathing 100% oxygen does not fully oxygenate the blood.[1] EFFECTS OF PPV CONT. Respiratory rate, VT, Inspiratory time, and flow rate can be controlled May cause stress ulcers and bleeding in GI tract COMPLICATIONS OF MECHANICAL VENTILATION High pressures are associated with barotrauma Pneumothorax, pneumomediastinum, pneumopericardium, subcutaneous emphysema Pneumothorax has decreased chest movement, hyperresonance to percussion, on affected side If tension pneumothorax: medical emergency Relieved by needle insertion, then chest tube Use 100% oxygen to speed reabsorption. 16 Complications related to pressure Ventilator-associated lung injury (VALI) DETERMINATION OF SETTINGS ON THE MECHANICAL VENTILATOR Placing patient on CMV Establish airway Select VT 8-12ml/kg of ideal body weight Select mode - a/c sensitivity at minimal to not self cycle Set pressure limit 10cmH2O above delivery pressure Set sigh volume 1-1/2 to 2 times VT Sigh pressure 10cmH2O above sigh delivery pressure Rate as ordered PEEP as ordered: exp. resist, insp. hold, etc. Set spirometer 100 cc less than patient volume check for function (turn on) Modes Control All of WOB is taken over by ventilator Sedation is required Control mode is useful During ARDS, especially if high PEEP is required or inverse I:E ratio Assist Patient is able to control ventilatory rate Should not be used for continuous mechanical ventilation if pt is apneic Assist/control Pt able to control vent rate as long as spontaneous rate > backup rate Machine performs majority of WOB Sedation is often required to prevent hyperventilation Is useful during early phase of vent support where rest is required Useful for long term for pt not ready to wean SIMV In between positive press breaths pt can breathe spontaneously Useful for long term for pt not ready to wean Used as weaning technique for short-term vent dependent pt PS Vent functions as constant pressure generator Positive pressure is set Pt initiates breath, a predetermined pressure is rapidly established Pt ventilates spont, establishes own rate, VT, peak flow and I:E Can be used independently/CPAP/SIMV Indicated to reduce work imposed by ETT, 5 to 20cm H2O Can be used for weaning A set IPS (12ml/kg VT) achieved by adjusting IPS level then slowly reducing as clinical status improves To overcome resistance of ETT, IPS should meet Raw To determine amount of PS needed: [(PIP – Plateau pressure) / Ventilatory inspiratory flow] x spontaneous peak inspiratory flow IBW Estimated ideal body weight in (kg) Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet. Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 fee. 1 Kilogram = 2.20462262 Pounds MONITORING CMV Observation Look at patient! Make a good visual assessment Start with patient, trace circuit back to ventilator Check and drain tubing Check connections Check patient Suctioning, position, etc. BP Spontaneous RR Heart rate and all vital signs Check machine settings VT (set, exhaled, corrected) f (assisted, set, spontaneous) Pressure limit: 10 above delivery pressure PEEP if applicable: Check BP! Peak Insp. Pressure (PIP): Keep as low as possible I:E ratio for proper flow FiO2: Keep as low as possible to prevent Oxygen Toxicity yet keep them adequately oxygenated Check all apnea alarms and settings. Check set VT to exhaled VT for any lost volumes If difference is greater than 100 cc, check for leak. Compliance Measures distensibility of lung – how much does the lung resist expansion. Relationship between Volume and Pressure High compliance equals lower PIP thus easier ventilation and less side effects of CMV Disease states resulting in low compliance include the Adult Respiratory Distress Syndrome (ARDS), pulmonary edema, pneumonectomy, pleural effusion, pulmonary fibrosis, and pneumonia among others. Emphysema is a typical cause of increased lung compliance. YOU MUST KNOW Dynamic = VT (corrected or exhaled) PIP – PEEP Always subtract out PEEP Consistently use exhaled or corrected VT Used to assess volume/pressure relationships during breathing – any changes in RR will effect it CDYN decreases as RR increases which may cause V/Q mismatch which may cause hypoxemia May reflect change due to change in flow due to turbulence instead of compliance Normal = 30 – 40 cmH2O VERY IMPORTANT Static = VT (corrected or exhaled) Plateau – PEEP Always subtract out PEEP Always consistently use either VT exhaled or VT corrected Will not change due to change in flow, more accurate Measured pressure to keep airways open with no gas flow. Normal values very with pt, but usually above 80 cmh2o will show lung overdistention Importance to follow trends in patient compliance Decreased C = stiffer lung = less compliant = higher ventilating pressures = you need a ventilator with high internal resistance to deliver volumes using square wave. High compliance = possible Emphysema STATIC VS DYNAMIC COMPLIANCE Decrease in CDYN with no change in CST indicates worsening airway resistance Causes Bronchospasm Secretions Kinked/Occluded ETT Inappropriate flow and/or sensitivity settings If both CDYN and CST worsen, not likely to be an airway problem Causes Pulmonary Edema ARDS Tension Pneumothorax Atelectasis Fibrosis Pneumonia Obesity Patient Position RAW = PIP – Pplat Flow (L/sec.) Airway Resistance Impedance to ventilation by movement of gas through the airways thus the smaller the airway the more resistance which will increase WOB (causing respiratory muscle and patient fatigue) Example: ETT, Ventilator Circuit, Bronchospasm Airway Resistance & Compliance Decreased Compliance + Increased Airway Resistance = High PIP, Decreased Volumes and significant increase in WOB Very difficult to wean a patient until problems are resolved PATIENT STABILITY Vital signs Pulse – normal, weak, thready, bounding, rate, etc. BP – hypo/hypertensive – directly related to CO Respirations – tachypnea, bradypnea, hyperpnea, hypopnea, rate, etc. Color – dusky, pale, gray, pink, cyanotic Auscultation - bilateral, etc. Are they bilateral, amount of air moving, rales, rhonchi or wheezing Are they Vesicular (normal) or Adventitious (abnormal) Describe what you hear: fine, course, high-pitched, lowpitched, etc. And the location where you heard it: bilateral bases, posterior bases, right upper anterior lobe, laryngeal, upper airway, etc. HEMODYNAMIC MONITORING BTFDC Also known as Balloon Tipped Flow Directed Catheter Swan-Ganz Catheter Pulmonary Artery Catheter Done by inserting a BTFDC into R atrium, thru R ventricle, and into pulmonary artery SvO2 is drawn from the distal port of a BTFDC Used to monitor tissue oxygenation and the amount of O2 consumed by the body CATHETERS AND INSERTION SITES PA PRESSURE WAVEFORMS CVP Monitors fluid levels, blood going to the right side of heart Normal = 2 – 6 mmHg (4 – 12 cmH2O) Increased CVP = right sided heart failure (cor pulmonale), hypervolemia (too much fluid) Decreased CVP = hypovolemia (too little fluid), hemorrhage, vasodilation (as occurs with septic shock) PAP Pulmonary Artery Pressure = B/P lungs Monitors blood going to lungs via Swan-Ganz catheter (BTFDC) Normal 25/8 (mmHg) Increased PAP= COPD, Pulmonary Hypertension, or Pulmonary Embolism PCWP Pulmonary Capillary Wedge Pressure monitors blood moving to the L heart Balloon is inflated to cause a wedge Normal PCWP = 8 mmHg Range is 4 – 12 mmHg Increased PCWP = L heart failure, CHF Measure backflow resistance Cardiac Output Expressed as QT or CO (QT= Greek alphabet, 1050 BC scientist used qt had cardiac output expression) Normal = 5 LPM Range 4 – 8 LPM Decreased CO = CHF, L heart failure, High PEEP effects I&O Needs to be monitored closely to prevent fluid imbalance due to increased ADH production and decreased renal perfusion Fluid imbalance can develop into pulmonary edema and hypertension CARDIAC OUTPUT (CO) The amount of blood pumped out of the left ventricle in 1 minute is the CO A product of stroke volume and heart rate Stroke volume: amount of blood ejected from the left ventricle with each contraction Normal stroke volume: from 60 to 130 ml Normal CO: from 4 to 8 L/min at rest Fick CO: Vo2/Cao2-Cvo2 C(a-v)O2 could decrease if CO is increased due to less oxygen needs to be extracted from each unit of blood that passes Fick Method The Fick method requires that you be able to measure the A-V oxygen content difference and requires that you be able to measure the oxygen consumption. An arterial blood gas from a peripheral artery provides the blood for the CaO2 measurement or calculation while blood from the distal PA port of a Swan-Ganz catheter provides the blood for the CvO2 measurement or calculation Dilution methods mathematically calculate (using calculus) the cardiac output based on how fast the flowing blood can dilute a marker substance introduced into the circulation normally via a pulmonary artery catheter. (injecting a dye in prox port of Swanz. Not really used anymore due to infections MEASURES OF CARDIAC OUTPUT AND PUMP FUNCTION •CARDIAC INDEX (CI) •Determined by dividing the CO by body surface area •Normal CI is 2.5 to 4.0 L/min/m2 •CI measurement allows a standardized interpretation of the cardiac function •True cardiac output compared to each persON MEASURES OF CARDIAC OUTPUT AND PUMP FUNCTION (CONT’D) Cardiac work A measurement of the energy spent ejecting blood from the ventricles against aortic and pulmonary artery pressures It correlates well with the amount of oxygen needed by the heart Normally cardiac work is much higher for the left ventricle MEASURES OF CARDIAC OUTPUT AND PUMP FUNCTION (CONT’D) Ventricular stroke work A measure of myocardial work per contraction It is the product of stroke volume times the pressure across the vascular bed Ventricular volume Estimated by measuring end-diastolic pressure Measures of Cardiac Output and Pump Function (cont’d) Ejection fraction The fraction of end-diastolic volume ejected with each systole; normally 65% to 70%; drops with cardiac failure DETERMINANTS OF PUMP FUNCTION Preload Created by end-diastolic volume The greater the stretch on the myocardium prior to contraction the greater the subsequent contraction will be When preload is too low, SV and CO will drop This occurs with hypovolemia Too much stretch on the heart can also reduce SV Determinants of Pump Function Afterload Two components: peripheral vascular resistance and tension in the ventricular wall Created by end systolic volume Increases with ventricular wall distention and peripheral vasoconstriction As afterload increases, so does the oxygen demand of the heart Decreasing afterload with vasodilators may help improve SV but can cause BP to drop if the blood volume is low Ventilation Patient Parameters Spontaneous VT Is it adequate for patient? Spontaneous volumes should be between 5 – 8 ml/Kg of Ideal Body Weight (IBW) Spontaneous VC 10 – 15 ml/Kg IBW NIF/MIP/MIF/NIP -20 to -25 cmH2O within 20 seconds ABGS PaO2 represents oxygenation – adjust with PEEP or FiO2 PaCO2 represents ventilation – adjust with VT or RR pH represents Acid/Base status pH acid: High CO2 (respiratory cause) or low HCO3 (Metabolic cause) pH alkaline: Low CO2 (respiratory cause) or high HCO3 (Metabolic cause) Draw ABGs To stabilize With any change in ventilator settings change only one vent setting at a time With any change in patient condition VENTILATOR ALARMS Appropriate for each patient Usually 10 higher/lower than set parameter For pressure and RR settings VT alarms 100 ml higher/lower than set VT Adjust all alarms for patient safety. X-RAY WHEN INDICATED FOR Tube placement: 2 – 4 cm above carina Possible pneumothorax To check for disease process reversal, or lack of, for treatment purposes and weaning FREQUENCY OF VENTILATOR CHECKS Must be done as often as required by the patients condition unstable patients continuous to hourly In general patients and ventilators need evaluation Q1-Q4h With every vent check, patient assessment should take place Use VT exhaled for calculations. Corrected VT = exhaled vt-tubing lost volume Tubing volume lost factor 1-8 cc x pressure Exhaled vt 650= pip-peep x (3) = 60 650-60=590 corrected vt WAVEFORM ANALYSIS Three wave forms typically presented together Pressure Flow Volume Plotted versus time Horizontal axis is time Vertical axis is variable Other common wave forms: Pressure vs Volume Flow vs Volume Pressure vs Time Assessment Patient Effort: Negative pressure deflection at beginning of inspiration indicates patient initiated breath Peak & Plateau Pressures Adequacy of inspiratory flow: If pressure rises slowly, or if curve is concave, flow is inadequate to meet patient’s demand. Flow vs Time Assessment Inspiratory flow patterns Air Trapping – a.k.a. AutoPEEP – expiratory flow fails to reach baseline prior to delivery of next breath Airway Resistance Lower slope (smaller angle) indicative of high resistance to flow Steeper slope (greater angle) indicative of lower resistance to flow Also increased resistance manifests itself as decreased peak expiratory flowrate (depth of expiratory portion of flow pattern) with more gradual return to baseline as expiratory flow meets with resistance Bronchodilator = increased peak expiratory flow rate with quicker return to baseline Volume vs Time Assessment VT = peak value reached during inspiration Air Trapping = fails to reach baseline before commencement of next breath Identifying breath type Larger volumes = mechanical breaths Smaller volumes = spontaneous breaths Pressure vs Volume Loop Volume on vertical axis Pressure on horizontal axis Positive pressure on right of vertical axis Indicates mechanical breath Application of positive pressure to the lung Tracing is in a “counter-clockwise” rotation Subambient pressure to the left of the vertical axis Indicates a spontaneous breath Spontaneous inspiration is to the left of the vertical axis – subatmospheric pressure at start of inspiration (Intrapulmonary pressure = -3 cmH2O) Spontaneous expiration is to the left of the vertical axis – +3 cmH2O intrapulmonary pressure on expiration Tracing is in a “clockwise” rotation Useful in helping diagnosing Alveolar Overdistension = looks like bird’s beak, or the “Partridge Family” symbol Increased RAW = looks “pregnant” or “fat” Decreased compliance = looks “lazy” or like it’s lying down Flow vs Volume Loop Helpful in assessing changes in RAW, such as after the administration of a bronchodilator Flow on vertical axis Volume on horizontal axis Inspiration is top part of loop, expiration on bottom When RAW improved, expiratory flows are greater and the slope of the expiratory flow is greater To determine patient effort, use the following curves Pressure vs Time Pressure vs Volume Loop Volume vs Time All show subambient drops in pressure/volume when patient initiates the breath To determine Auto-PEEP, use Volume vs Time Flow vs Time Pressure vs Volume Loop For all curves, ask “does the exhalation reach baseline before the next breath starts To determine the adequacy of inspiratory flow Pressure vs Time = concave or slow rise to pressure means inadequate flow on inspiration Volume vs Time = Too slow flow = increased I – Time = decreased E-Time = AutoPEEP Volume vs Pressure = Slope is shallow, may look similar to loop associated with increased RAW If you detect the patient actively working during mechanical breath, increase the flow to help meet the patient’s demand and decrease the WOB To assess changes in compliance, use Pressure vs Volume Loop Steeper slope = increased compliance, or larger volume at lower pressure Shallow slope = decreased compliance, or smaller volume at higher pressure To assess changes in RAW, use Pressure vs Volume Loop Space – “hysteresis” – between inspiratory and expiratory portions of loop “Bowed” appearance – inspiratory portion more rounded and distends toward the pressure axis Flow vs Volume Loop Observe peak flow on Flow-Volume Loop Increased RAW = Decreased Peak Flow UNIT B Acute & Critical Care PEEP/CPAP PEEP – Positive End Expiratory Pressure Definition Application of pressure above atmospheric at the airway throughout expiration Goal To enhance tissue oxygenation Maintain a PaO2 above 60 mmHg with least amount of supplemental oxygen Recruit alveoli Indications Cardiogenic pulmonary edema Left sided heart failure Prevents transudation of fluid Improves gas exchange ARDS Increases lung compliance Decreases intrapulmonary shunting Increases FRC Refractory hypoxemia PaO2 < 50 mmHg with an FIO2 >50% Increase FRC Opens collapsed alveoli Increases reserve Contraindications Unilateral lung disease Hypovolemia Hypotension Untreated pneumothorax Increased ICP Hazards All of the effects of CMV are magnified Increased intrathoracic pressure Decreased venous return Increased ADH Decreased blood pressure Decreased cardiac output Loss of thoracic pump Barotrauma Physiological effects Baseline pressure increases Increased intrapleural pressures Increased FRC—recruiting collapsed alveoli Dead space—increased in non-uniform lung disease and healthy lungs by distending alveoli Increased alveolar volumes Can increase compliance Cardiovascular Decrease venous return Decrease cardiac output Decrease blood pressure Decreases intrapulmonary shunt Increases mixed venous value (PvO2)--Drawn from pulmonary artery via Swan-Ganz Increased intracranial pressures Decrease in A-a gradient (A-a DO2) Increased PaO2 Decrease in FIO2, which causes a decrease in PAO2 INITIATION AND MONITORING OF PEEP Start off at 5 cmH2O and increase by 3 to 5 cmH2O increments Adjust sensitivity With an increase in baseline pressure the sensitivity must be increased or the patient will have to increase inspiratory effort to initiate a breath Monitor Blood pressure: First thing you look at when adding PEEP Cardiac output: Goal is least cardiac embarrassment with the best PaO2 and least FIO2 Pulse If the patient is hypoxemic their heart rate is probably increased With addition of PEEP the hypoxemia should resolve and pulse should decrease to normal level PaO2: Goal is best PaO2 with the lowest possible FIO2 MAINTENANCE LEVEL OF PEEP PEEP trial Used to determine best level of PEEP This is the pressure at which cardiac output and total lung compliance is maximized,the VD/VT is minimal, and the best PaO2 and PvO2, and the lowest P(A-a)O2 are obtained 1. Best PEEP or Optimum PEEP Level at which physiological shunt (Qs/Qt) is lowest without detrimental drop in cardiac output A C(A-V)O2 of less than 3.5 vol% should reflect adequate CO Fick’s law CO = VO2/C(a-v)O2 Cardiac output and C(a-v)O2 are inversely related 2. Optimal PEEP Level which provides maximal O2 delivery(DO2) and lowest VD/VT Cardiac output can often be compromised but not concerned with if using optimal PEEP CPAP Physiologically the same as PEEP Used in spontaneously breathing patients Maintains continuous positive airway pressure during inspiration and expiration Accomplished by a continuous flow of gas or a demand valve Used to treat OSA System flow must be enough to meet patient’s peak inspiratory demands CPAP delivered via mask or nasal pillows No machine breaths, all spontaneous ventilation NPPV (BIPAP) Similar to CPAP Delivers two levels of pressure during the inspiratoryexpiratory cycle Delivers higher pressure on inspiration Delivers lower pressure on exhalation Less resistance to exhalation Two levels of pressure EPAP Constant pressure delivered during exhalation Same as CPAP Adjust for oxygenation IPAP Constant pressure delivered during inspiration Same as IPPB Adjust for ventilation The difference between the two pressures is known as pressure support Used to treat OSA Better tolerated than traditional CPAP Delivered with mask or nasal pillows Used in acute respiratory failure Can prevent or delay intubation and CMV Improves ventilation and oxygenation Improves patient comfort RULES OF PUTTING PATIENT ON PEEP Obtain order Set-up PEEP and make additional changes (i.e., sensitivity) Monitor patient for hazards, BP, CO if available Monitor for "optimum PEEP" Decrease FIO2 as possible until below 0.40-.50, then decrease PEEP IMV/SIMV Definitions IMV: Intermittent Mandatory Ventilation Patient receives set number of mechanical breaths from the ventilator. In between those breaths, the patient can take their own spontaneous breaths at a rate and VT of their choice. SIMV: Synchronized Intermittent Mandatory Ventilation Same as IMV, except the mechanical breaths are synchronized with the patient’s spontaneous respiratory rate. Helps improve patient/ventilator synchrony and helps prevent “breath stacking” (where the vent delivers the machine set VT on top of the patient’s spontaneous VT) IMV Advantages Prevents muscle atrophy – makes patient assume an increasing, self-regulating role in their own respirations, helping to rebuild respiratory muscles Allows patient to reach baseline ABGs – baseline means the patient’s baseline ABGs Chronic CO2 retainer ABGs do not have a normal PaCO2 of 40 Decreases mean intrathoracic pressure – the lower the IMV/SIMV rate, the lower the intrathoracic pressure Avoids decreased venous return – lower intrathoracic pressure = greater venous return Avoids cardiac embarrassment – greater venous return = less decrease in cardiac output and blood pressure PEEP devices Water column Amount of water in a column determines PEEP Pressure in expiratory limb must exceed pressure of water in column Exhalation occurs under a Column of water Spring loaded valve: Tension in spring determines PEEP Balloon type Similar to “mushroom-type” exhalation valve Balloon is in exhalation valve Balloon is inflated to a given pressure Pressure in balloon determines PEEP Diaphragm Pressure against diaphragm Disposable circuit with MA-1 May avoid positive fluid balance Allows normalization of ADH production Helps avoid cardiac embarrassment Psychological encouragement Some patients may exhibit anxiety, especially those who have been on the vent for several days or weeks Do not tell the patient they will never need the vent again Some patients become encouraged by progress, being able to do more for themselves Weaning gradually – re-evaluate if weaning takes several days May allow decreased use of pharmacological agents – e.g., morphine, diprivan, versed, etc. If patient is too sedated, won’t be able to breathe spontaneously and participate in weaning May be the only way to correct respiratory alkalosis on patient who is “over-breathing” the vent in A/C mode Patient’s spontaneous VT will most likely be smaller than that of the set VT on mechanical ventilator Candidates for IMV/SIMV IMV/SIMV is great for weaning patient from CMV Allows patient to assume increased responsibility for providing own respirations, with diminishing mechanical support Allows patient to re-build respiratory muscle strength Patient must be stable. Not ideal for unstable patient. Consider patient unstable if Fever – causes increased O2 consumption and increased CO2 production, thereby increasing WOB Unstable cardiac status Unresolved primary problem that caused them to be on the vent in the first place Problems of IMV Fighting the ventilator – patient becomes out of phase – or synch – with the ventilator Stacking of breaths is not necessarily a problem Patient will normally synchronize self with ventilator rate Patient disconnection from gas source (with external IMV circuit) Other problems of CMV Benefits of SIMV – Synchronized IMV Prevents stacking of breaths (pt can breath spontaneously through demand valve) May help patient to become in phase with vent Breath stacking could be prevented just by increase inspiratory flow INSPIRATORY PRESSURE SUPPORT (IPS) Commonly referred to simply as “Pressure Support” During spontaneous breathing, the ventilator functions as a constant pressure generator Pressure develops rapidly in the ventilator system and remains at the set level until spontaneous inspiratory flow rates drop to 25% of the peak inspiratory flow (or specific flow rate) This mode may be used Independently With CPAP With SIMV With any spontaneous ventilatory mode Not with any full support modes, such as Control or A/C PS is used to overcome the increased resistance of the ET tube and vent circuit Pouiselle’s Law: decrease the diameter of a tube by ½, increase the resistance of flow through that tube by 16 times If you apply/use PS, do not set less than 5 cmH2O of PS — least amount needed to overcome resistance of ET tube and vent circuit If PS is set at a level higher than RAW, you will be adding to patient volumes, rather than just helping overcome the increased resistance from the ET tube and vent circuit Can be used to help wean patient from vent and help rebuild respiratory muscle strength MANAGEMENT OF VENTILATORS BY ABGS Pressure Control Ventilation Can be used as CMV or SIMV In SIMV mode, the machine breaths are delivered at the preset pressure while the spontaneous breaths are delivered with PS PC-CMV (a.k.a., PCV) used to decrease shear forces that damage alveoli whenever the peak or plateau pressures meet or exceed 35cm H2O Help prevent damage to alveoli from excessively high ventilating pressures Shear forces damage alveoli when they collapse (because closing volumes are above FRC) and then are forced back open again with the next breath. Damage occurs as this cycle is repeated over time: alveoli collapses, then is reinflated, collapses, reinflated, etc. Also used when permissive hypercapnia is desired (treatment of ARDS) When the PaCO2 is allowed to rise through a planned reduction in PPV, which allows for a reduction in the mean intrathoracic pressure, which results in less incidence of barotrauma and other commonly associated complications of PPV The gradual increase in PaCO2 is accomplished by a reduction of the mechanical VT (by decreasing the pressure) and usually does not affect the oxygenation PC-IRV: Pressure Controlled Inverse Ratio Ventilation Pressure controlled ventilation with an I:E ratio > 1:1. Causes mean airway pressure to rise with the I:E ratio Usually used on patients with severe hypoxemia where high FIO2s and PEEP have failed to improve oxygenation Causes intrinsic PEEP (a.k.a. auto-PEEP), which is what causes the mean airway pressure to increase, which is the mechanism for alveolar recruitment and improved arterial oxygenation While an increase in oxygenation does occur at the lung, a resultant decrease in cardiac output (due to the increased mean intrathoracic pressures) may result in an overall decrease in tissue oxygenation. Care must be exercised to maintain adequate cardiac output in order to maintain adequate tissue oxygenation Because it’s not a natural way to breath (backwards from the way we normally breath), most patients must be either heavily sedated (Diprivan, Versed) or must be paralyzed with a paralytic drug (such as Pavulon or Norcuron) APRV: Airway Pressure Release Ventilation Related to PC-IRV except that patient breathes spontaneously throughout periods of raised and lowered airway pressure. APRV intermittently decreases or releases the airway pressure from an upper CPAP (IPAP) level to a lower CPAP (EPAP) level The airway pressure release usually lasts 1.5 seconds or shorter, allowing the gas to passively leave the lungs to eliminate CO2 I:E ratio is usually > 1:1, but differs from PC-IRV in that it allows spontaneous breathing Because patient is breathing spontaneously, there is less need for sedation Usually has lower peak airway pressure than PC-IRV Originally proposed as a treatment for severe hypoxemia, but appears to be more useful in improving alveolar ventilation rather than oxygenation. END TIDAL CO2 MONITORING (PETCO2) Measures CO2 level at end exhalation, when CO2 levels are highest in exhaled breath Two methods of collection Sidestream – typically used for non-intubated patients Mainstream – typically used for intubated patients and more commonly seen and used Probe is placed between the patient wye of vent tubing and the patient’s ETT Infrared light measures CO2 levels Inspired gas should have value of zero PETCO2 content should be within 2 – 5 mmHg of patient’s PaCO2 Difference will be greater on a patient with larger amounts of air trapping, e.g. Emphysema CAPNOMETRY (CONT.) 96 End-tidal CO2 monitoring is for trending Not absolute—can vary from breath to breath; similar to pulse oximetry Look at the trend. Is the patient’s PETCO2 increasing or decreasing over a period of time? Similar activity should then be also occurring with the PaCO2 When setup, correlate the PETCO2 readings with current ABGs PaCO2. This will give you an idea of how much less the PETCO2 is reading than the PaCO2, giving you a good idea of future trends of the PETCO2 will relate to the PaCO2 CHEST TUBE DRAINAGE SYSTEMS Chest tube placed high in thoracic cavity to drain air Second or third intercostal space at midclavicular line Incision made right over the rib Chest tube advanced towards anterior apex of lung. Chest tube placed low in thoracic cavity to drain fluid (e.g., pleural effusion) Placement is in fourth intercostal space (or lower) at midaxillary line Patient is placed lying on side with affected side “up” Once incision is made, tube is advanced posteriorly, toward the base of the lung so gravity can help drain the fluid Three chamber chest tube drainage system is most common Left chamber is the suction control chamber Level of water determines how much suction is applied to the chest cavity, regardless of how much the suction is set on the suction regulator on the wall Middle chamber is the water seal chamber Usually no more than 2 cmH2O Too much and you increase difficulty of air or fluid to drain Too little and you risk an air leak Bubbles in water seal indicate that a leak in the lung is still present Spontaneous breathing patients with leak will have bubbles on exhalation Intubated, mechanically ventilated patients with leak will have bubbles on inspiration Continuous bubbling could be a sign of a leak in your chest tube drainage system and must be corrected immediately! Clamp chest tube briefly where it exits patient’s chest. If bubbling stops, leak is in your patient (intrathoracic). If bubbling persists, then you must check your chest tube drainage system for leaks Move clamp down tubing in 10cm (approx. 4 inch) increments (working from patient to chest tube drainage system), briefly clamping as you go until bubbling stops Right chamber is the drainage collection chamber This is where the fluid drained from the patient is collected ALI=ACUTE LUNG INJURY OR ARDS Definition agreed upon in 1994 at the American – European Consensus Conference on ARDS ALI Definition: a syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterized by: Bilateral radiographic infiltrates A ratio PaO2/FIO2 between 201 and 300 mmHg, regardless of the level of PEEP. The PaO2 is measured in mmHg and the FIO2 is expressed as a decimal between 0.21 and 1.00 No clinical evidence of an elevated left atrial pressure. If measured, the PCWP is 18 mmHg or less ARDS Definition: same as ALI, except the hypoxia is worse. Requires a PaO2/FIO2 ratio of 200 mmHg or less, regardless of the level of PEEP. ARDS is ALI in its most extreme state Mortality rate between 40 and 60% -- varies from source to source Down from about 20 years ago when ARDS was almost certain death sentence with approximately 90% mortality rate. Current Protective Lung Strategies Lower VTs with ALI/ARDS patients: about 4-6 ml/Kg IBW to avoid “volutrauma” from alveolar over distension Sufficient PEEP to prevent alveolar collapse at end expiration, yet not so much that cardiac status is compromised Permissive hypercapnia when treating ALI/ARDS PaO2 > 65 mmHg PIP < 35cm H2O If your PIP is greater than 35cm H2O, consider using PCV Closed suctioning system to maintain PEEP Do not “bag” ALI/ARDS patient to “recruit more alveoli”; could lead to barotrauma or volutrauma Monitor: Patient must be monitored closely as condition can change relatively quickly! Things to monitor: I&O Cardiac output BP PIP PPLAT Pulse Ox FIO2 VT VE CST PETCO2 Waveforms A-a Gradient Renal vasoconstriction, due to hypoxemia, reduces urinary output. Resolution of the hypoxemic state relieves the renal vasoconstriction, thus increasing urinary output. MANAGEMENT OF ABGS WITH CMV ABG normal pH values Normal range = 7.35 – 7.45 “Normal” = 7.40 PaCO2 High PaCO2 will cause a low pH, thus causing respiratory acidosis Low PaCO2 will cause a high pH, thus causing respiratory alkalosis pH needs to be corrected so that drugs being given to patient will be metabolized PaCO2 and Ventilation ABG normal PaCO2 values PaCO2/Ventilation = 35 – 45 “Normal” = 40 High PaCO2 represents hypoventilation or the patient is under ventilated or retaining CO2 Low PaCO2 represents hyperventilation or the patient is over ventilated or blowing off CO2 CO2 represents how well your patient is ventilating. You would adjust VT, f, or remove dead space if on ventilator PaCO2 & pH Calculations PaCO2 and pH have a direct relationship. Starting at a PaCO2 of 40 If PaCO2 increases by 20 mmHg, pH decreases by 0.10 If PaCO2 decreases by 10 mmHg, pH increases by 0.10 To increase PaCO2 decrease VA The PaCO2 is inversely proportional to VA providing that CO2 production remains constant VA = (VT – VD)f To decrease VA (increase PaCO2) Decrease VT (keep in normal range) Decrease f (will not blow off as much CO2) Increase VD (only in control mode – 50cc per link of large bore tubing) To decrease PaCO2 increase VA VA = (VT – VD)f To increase VA (decrease PaCO2) Increase VT (keep in normal range) Increase f (will blow off more CO2) Decrease VD Dead Space = Ventilation without perfusion Anatomical dead space averages about 1 ml per pound Alveolar dead space is alveoli that are ventilated but not perfused Physiological dead space is the sum of the above Normally, this is approximately 1/3 of the VT, or between 20 and 40% for spontaneously breathing, non-intubated patient Normal for patient on ventilator is 40 – 60% Formulas for VD/VT, Desired VT, & Desired f VD/VT = PaCO2 – PetCO2 PaCO2 Gives the portion/percentage of VT not taking place in gas exchange. STRATEGIES TO ALTER VENTILATION Always adjust VT first, but remember to keep it in the normal range (8 – 12 ml/kg of ideal body weight) If PaCO2 is high, patient is on SIMV, and the patient is taking spontaneous breaths and the volumes are low, initiate Pressure Support to increase spontaneous volumes. If you cannot adjust VT up or down because it would place the VT out of normal range, then change f (rate) Change Mechanical Rate Doing this alters Alveolar Ventilation If your rate exceeds 20 bpm, auto-PEEP may develop (patients with very stiff lungs. e.g., ARDS—may require higher f) Increase f = decreased PaCO2 (hyperventilate) Decrease f = increased PaCO2 (hypoventilate) Add or remove VDMech only in control mode Add VDMech to increase PaCO2 Decrease VDMech to decrease PaCO2 Cut ETT to proper length to decrease dead space Use low compliance vent circuit to decrease dead space Large VT and slow f are preferred to small VT and rapid f because Alveolar Ventilation is increased Distribution of inspired gas is improved Ventilation/Oxygenation is improved Mean intrathoracic pressure is reduced PAO2 & OXYGENATION PaO2/Oxygenation norm = 80 – 100 If PaO2 is below 60, the patient has hypoxemia For patients that are hypoxic and on a ventilator, adjust the FIO2 to > 50% then start adding PEEP When the patient improves, decrease FIO2 to 40 – 50%, then start removing PEEP to prevent O2 toxicity To increase PaO2 (in any mode) Increase FIO2 if hypoxemia is caused by low V/Q ratio to > 50, then add PEEP to prevent oxygen toxicity. When hypoxemia is present due to lung injury or physiological shunting (as in disease states like ARDS), go up to 100 and then add PEEP or CPAP TWO INDICES OF OXYGENATION a/A Ratio PaO2/PAO2 O2 from alveoli to blood Divide PaO2 by PAO2 Normal = > 60% A-a Gradient P(A-a)O2 Difference between alveolar and arterial PO2 Subtract PaO2 from PAO2 Normal: - On 21%: 10 – 15 - On 100%: 65 On 100%, every 50 mmHg difference equals approx. 2% shunt If under 300, you have V/Q mismatch so increase FiO2 If over 300, you have a shunt, so add PEEP or CPAP First calculate PAO2 Unless told otherwise PBAR = 760 PH2O = 47 RQ = 0.8 (Pb-PH2O)fio2-(Paco2x1.25) If FiO2 is greater than 60%, omit RQ from PAO2 formula PaO2 is obtained from an ABG To decrease PaO2 (in any mode) Decrease FIO2 Decrease PEEP gradually If FIO2 > 50% with PEEP, decrease FIO2 to 40 – 50% first (to reduce O2 toxicity) If patient remains stable and has an adequate PaO2, start to reduce PEEP slowly Monitor patient at all times for signs of hypoxemia MANIPULATION OF ABGS IN CONTROL MODE To increase PaCO2 Decrease VT Decrease f Increase VD To decrease PaCO2 Increase VT Increase f Decrease VD MANIPULATION OF ABGS IN A/C To increase PaCO2 Decrease VT: May be ineffective as pt. may increase f Decrease f: Patient can increase assisting to override Never add VD in any mode but control To decrease PaCO2 Increase VT Increase f above assist rate If ineffective, change to control or IMV modes MANIPULATION OF ABGS IN SIMV/IMV To increase PaCO2 Decrease VT – only to ranges for patient Not best choice Decrease f Best choice towards weaning Never add VD in this mode Will increase patient’s WOB and they will eventually fail To decrease PaCO2 Increase VT - stay within normal range Increase f (blow off CO2) Increase minute ventilation May need to add PS to augment spontaneous volumes Do not look at just the numbers and values Always assess your patient with every ventilator change. You are treating a patient, not a machine!