-10- Critical Care

September-15-08 8:37 AM

There will be only 3 - 4 questions on this and they will be straight forward

Notes By:

Critical Care Medicine

Dr. Tim Ashburn, M.D., FCCP

VENTILATORS
CYCLING and MODES Ventilator Pic Cycling Mechanisms * Time cycled * Pressure cycled * Volume cycled * Flow cycled Parameters * Pressure: measure of impedance to flow (cm H2O ) * Volume: tidal volumes (mls or Ls) * Flow rate: rate of gas volume delivered ( L/s or L/min) * Time: I:E ratio This ventilator mode is giong to deliver a breath times volume or pressure come hell or high water, it will do it no matter what without patients control. We put these people in heavy sedation and comas.

MODES * Control Mechanical Ventilation (CMV)- Delivers preset volume or pressure regardless of patients own inspiratory efforts. Usually used for patients who are apneic. * Assist-Control Ventilation (A/C)-Delivers breath in response to patient effort and if patient fails to do so within preset amount of time. Usually used for spontaneously breathing patients with weakened respiratory muscles. * Synchronous Intermittent Mandatory Ventilation (SIMV)-Ventilator breaths are synchronized with patients respiratory effort. Usually used to wean patients from mechanical ventilation or to rest when used with high levels of PSV. * Pressure Support Ventilation (PSV)- Preset pressure that augments the patients inspiratory effort and decreases the work of breathing. Often used with SIMV during weaning Slide 4. Showing Pressure, Volume, Flow. You can put limit on these to prevent blowing the lung out.First Pressure Graph on top left: Negative inflection was sensed by the ventilator and it gave him extra breaths. Right column, instead of volume control, it has pressure control. IMV pressure control with pressure support. That is an example of IMV pressure control with pressure support. * Positive End Expiratory Pressure (PEEP)-Positive pressure applied at the end of expiration. Used with CMV, A/C, and SIMV to improve oxygenation by opening collapsed alveoli and keeping them open * Constant Positive Airway Pressure (CPAP)-Similar to PEEP but used only with spontaneously breathing patients. Maintains constant positive pressure in airways so resistance is decreased * Independent Lung Ventilation (ILV) -Ventilates each lung separately; requires two ventilators and sedation/paralysis. Used for patients with unilateral lung disease or different disease process in each lung * High Frequency Ventilation (HFV)- Delivers small amounts of gas at a rapid rate (60-100 breaths/minute); requires sedation/paralysis. Used for hemodynamic instability, during short-term procedures, or if patient is at risk for pneumothorax * Inverse Ratio Ventilation (IRV)- I:E ratio is reversed to allow longer inspiration; requires sedation/ paralysis. Improves oxygenation in patients who are still hypoxic even with PEEP; keeps alveoli from collapsing. Will result in permissive hypercapnia NIPPV/NIAV - non-invasive positive pressure mask Abbreviations in NIPPV / NIAV * AHRF Acute hypercapnic respiratory failure * CHRF Chronic hypercapnic respiratory failure * NIAV Non-invasive assisted ventilation * IPPB Intermittent positive pressure breathing * NIPPV Non-invasive positive pressure ventilation or nasal intermittent positive pressure ventilation * CPAP Continuous positive airways pressure * BiPAP Bi-level positive airways pressure * IPAP Inspiratory positive airways pressure * EPAP Expiratory positive airways pressure NIPPV / NIAV in AHRF * Is very effective in supporting ventilation in acute exacerbations of COPD leading to HRF and thus avoiding endotracheal intubation. * Can rapidly improve pH, pCO2 and pO2 * Can rapidly reduce level of breathlessness and is well tolerated by sick patients. * May reduce complication rate, hospital length of stay and reduce mortality. * Is not nurse intensive and can be performed safely on a general ward * Pt must be alert and able to protect their airway Initiation of Ventilatory Support Laboratory criteria * Blood gasesPaO2 <55 mm HgPaCO2 >50 mm Hg and pH <7.25 * Pulmonary function tests Vital capacity <10 mL/kg Negative inspiratory force <25 cm H2O Clinical criteria * Apnea or hypopnea * Respiratory distress with altered mentation * Clinically apparent increased work of breathing * Obtundation and need for airway protection Other criteria * Controlled hyperventilation (eg, in head injury) * Severe circulatory shock

In the Assis-Control, the machine will sense if the patient wants to breathe and they will add a few extra breaths a minute, etc. but its patient triggered

SIMV: if you set a patient here on a rate of 10 or 12 and they dont overbreathe, then everyone is the same as assist-control breaths, but in IMV, if they breathe over, then the ventilator does not assist them, so they have to breathe through all that tubing. (purpose defeated if you are trying to rest the patient). PSV: What we can do is put them in IMV, and set a rate of 8 or 10 or 12, and set a volume. Everyone of those breaths is the same. If they dont overbreathe, its just like assist-control. This one is much more physiologic, it will adjust the tidal volume to what their needs, airway resistance, chestallresistance, and muscle usage is.

For us, these two are essentially identical. Rpessure set at end of breath that keeps alveoli open. We want to recruit alveoli and keep them open. The difference is terminology and some techinical differences. If its a pressure support breath, initiated by the patient its a CPAP, but essentially they are the same. You can ventilate one lung at a time.

Theres something called High frequently ventilation. Never proven to work.

BiPAP can be used for sleep apnea. You have two levels of pressure with a mask. On inspiration you would set a level of 10-15 of pressure, but on the end you want to keep the alveoli open so you set a smaller level. Thats called bipap

Very well tolerated, can be done in stepdown ward, dont have to be in ICU, not as intensive as intubated patients. The absolute most important thing is they have to be alert in order to protect their airway. If they cant protect their airway, then intubate them. Protect so that they dont aspirate into their lungs.

Always ventilate the head trauma - hyperventilate them -> respiratory alkalosis -> vasoconstriction.

Mode of ventilation * The mode of ventilation should be tailored to the needs of the patient. In the emergent situation, the physician may need to order initial settings quickly. SIMV and A/C are versatile modes that can be used for initial settings. In patients with a good respiratory drive and mild-to-moderate respiratory failure, PSV is a good initial choice. Tidal volume

Think about what modes of ventilation do we want. Respiratory rate of 20-16 is tachypnea.

Take home message, rest:AC

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Tidal volume * Observations of the adverse effects of barotrauma and volutrauma have led to recommendations of lower tidal volumes than in years past, when tidal volumes of 12-15 mL/kg were routinely used. * An initial TV of 8-10 mL/kg of ideal body weight is generally indicated, with the lowest values recommended in the presence of obstructive airway disease and ARDS. The goal is to adjust the TV so that plateau pressures are less than 35 cm H2O. Respiratory rate * A respiratory rate (RR) of 10-12 breaths per minute is recommended for patients not requiring hyperventilation for the treatment of toxic or metabolic acidosis, or intracranial injury. High rates allow less time for exhalation, increase mean airway pressure, and cause air trapping in patients with obstructive airway disease. The initial rate may be as low as 5-6 breaths per minute in asthmatic patients when using a permissive hypercapnic technique. Supplemental oxygen therapy * The lowest FiO2 that produces an arterial oxygen saturation (SaO2) greater than 90% and a PaO2 greater than 60 mm Hg is recommended. No data indicate that prolonged use of an FiO2 less than 0.4 damages parenchymal cells.

Take home message, rest:AC TD: 12-15cc RR: 20: tachypnea, even 16 is tachypnea Generally you put someone on 100% 02 when you first intubate then you decrease.

Inspiration/expiration ratio * The normal inspiration/expiration (I/E) ratio to start is 1:2. This is reduced to 1:4 or 1:5 in the presence of obstructive airway disease in order to avoid air-trapping (breath stacking) and auto-PEEP or intrinsic PEEP (iPEEP). Use of inverse I/E may be appropriate in certain patients with complex compliance problems in the setting of ARDS. Inspiratory flow rates * Inspiratory flow rates are a function of the TV, I/E ratio, and RR and may be controlled internally by the ventilator via these other settings. If flow rates are set explicitly, 60 L/min is typically used. This may be increased to 100 L/min to deliver TVs quickly and allow for prolonged expiration in the presence of obstructive airway disease. Positive end-expiratory pressure * PEEP has been found to reduce the risk of atelectasis trauma and increase the number of "open" alveoli participating in ventilation, thus minimizing V/Q mismatches. * One obvious beneficial effect of PEEP is to shift lung water from the alveoli to the perivascular interstitial space. It does not decrease the total amount of extravascular lung water. This is of clear benefit in cases of cardiogenic as well as noncardiogenic pulmonary edema. An additional benefit of PEEP in cases of CHF is to decrease venous return to the right side of the heart by increasing intrathoracic pressure. * Applying physiologic PEEP of 3-5 cm H2O is common to prevent decreases in functional residual capacity in those with normal lungs. The reasoning for increasing levels of PEEP in critically ill patients is to provide acceptable oxygenation and to reduce the FiO2 to nontoxic levels (FiO2 <0.5). The level of PEEP must be balanced such that excessive intrathoracic pressure (with a resultant decrease in venous return and risk of barotrauma) does not occur. Initial Settings

Most of the time I:E ratio is set already.

This is what it looks like when we start writing our orders

SETTINGS * Mode / Rate / VT / FIO2 / PS / PEEP * Ex: SIMV / 12 / 700 / 60% / PS + 15 / +5 * Ex: A/C / 10 / 750 / 50% / +5 * Ex: IVRPVC / 12 / PC 35/ 100%/ I:E 2:1 / +10

This is how we write it. We need t oknwo these, need to learn ahow to interpret this. The mode comes first, by convention, then the rate, tidal volume, FIO2, pressure support, then the PEEP. If you overbreathe IMV with pressure support, then what you get is these smaller tidal volumes. In A/C, all the breathes are gpoing to be the same even if they overbreathe. This is what it would look like for someone with ARDs. We will flip the I:E ratio, 2 units of inspiration and 1 to out. (normal is 1:2, 1:3)

Beneficial CV Effects of PPV * Decrease LV afterload * Compress heart, aids ejection * Squeezes pulmonary Veins and augments LA filling * Decrease venous return, preloadreduction * Decrease work of breathing,WOB Side Effects and Complications * Spontaneous Breathing- Stacking breaths and bucking the vent * Barotrauma * Volutrauma * VAP * Auto-PEEP * O2 Toxicity

Patient gets out of sync from ventilator, or they get anxious and are not breathing together. So we must sedate patient. If we use high PEEP levels we can cause barotrauma If we use volume control, then volutrauma.

Weaning from SIMV/PS - When patient is triggering additional breaths, assure adequate exhaled VT ( >5ml/kg IBW) or 50% of the exhaled machine VT. If spontaneous volumes are too low, add pressure support (PS) at a level to achieve desired volume. * Wean SIMV by 2 BPM every 2-4 hours to a minimum of 6 BPM. * Watch exhaled minute volumes and observe for signs of intolerance. Check ABG's PRN to assure that the patients ventilatory and oxygenation requirements are being met. * Wean PS as appropriate to maintain spontaneous tidal volumes at the desired level. * Wean PEEP and FIO2 as tolerated while still maintaining SaO2% > 90% * When the PS and PEEP are # 5 cmH2O, and FIO2 is # 40%, initiate a CPAP trial for up to one hour. Observe the patient for tolerance of CPAP (i.e., VT > 5ml/kg IBW and adequate minute ventilation).

Never paralyze the patient unless they are sedated first

Rest the patients at night with ventilation, then in the daytime decrease the IMV to something like 4 and give them the rest as pressure support. See hwo they do for an hour.

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Observe the patient for tolerance of CPAP (i.e., VT > 5ml/kg IBW and adequate minute ventilation). If the patient tolerates the CPAP trial (trials should not exceed one hour), obtain weaning parameters and an ABG. Acceptable extubation values are as follows: * NIF > -30 cmH2O * Spontaneous VT >5mL/Kg ideal body weight * Respiratory rate < 30 * VC (if obtainable) >10mL/Kg ideal body weight * Minute ventilation < 10 L/min * pH > 7.30 * PaCO2 < 50 mmHg (unless patients baseline value is higher) * PaO2 > 60 mmHg on < 40% FIO2 . Room air oxygen is 20%. This is not saturation.

These are just guidelines, but its more of an art. Keep the oxygen above 60

ARDS
Adult Respiratory Distress Syndrome The Inexact Definition for ARDS Contributes to difficulty in management ARDS and ALI consensus statement definitions Acute onset (not specified) Fi02 ratio < 200 (300 for ALI) - Bilateral infiltrates on chest radiogrsph (highly variable) - PAWP < 18 mm Hg absence clinical evidence at volume overload

You have to meet all these components even though they are inexact. The way you get an FIO2 ratio is you get their oxygen content and you divide it by what ever FIO2 they are on. If someone is 100%, then you divide by 1. etc. You need to have a Pulmonary A WedgePressure of <18, otherwise we cant rule out pulmonary edema.

ARDS is a toxic hit to the lungs, it can come from many sources, but it starts intravascular. Imagine body taking a massive hit, what is the response? Inflammatory cells, mediators, just starts pouring all this stuff out. It frenchfries the lungs from the inside out. Then we lose the integrity from the endothelial barrier, then into the interstitial space, and epithelial barrier. Etc. Early on you have exudates, noninfectious, but exudates. If they live, they will fibrose. Here is a schematic of an alveolus normal and injured. In injured, you see edema in interstitial space, activation of neutrophil in alveoli, Chest Xray. How do we know this is not CHF with pulmonary edema? We dont. How do we know that it is not bilateral community acquired pneumonia? Wedont.Five things that fill up alveoli: Transudate, pus, pneumonia, blood (we cant say this is not acute pulmonary hemorrhage syndrome), cancer. Overpenetrated, mass Xray This is what it looks like on CT scan. Little overpenetrated but normal Look at the proteinaceous material on an atelectatic lung. You can see that you have some airspace disease there. This is how it progresses, you can see air bronchograms by CT. Look, the right lung is essentiall useless for ventilation CT ARDS * Frequency- 75/100,00 * Mortality- 30% to 70%, increases with age * Sex- no differences * History- acute onset, within 12-48 hrs of insult generally Terms * ARDS- Adult Respiratory Distress Syndrome * ALI- Acute Lung Injury Parsoei. * SIRS- Systemic Inflammatory Response Syndrome * MODS- Multiple Organs Dysfunction Syndrome P.E. * Physical: finding depend on underlying cause * Physical findings often are nonspecific and include tachypnea, tachycardia, and the need for high inspired oxygen concentrations to maintain oxygen saturation. * The patient may be febrile or hypothermic. * Because ARDS often occurs in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be present. * Cyanosis of the lips and nailbeds may occur. Examination of the lungs may reveal bilateral rales. * Manifestations of the underlying cause, such as acute abdominal findings in pancreatitis, are present. * In a septic patient without an obvious source, pay careful attention during the physical examination to identify potential causes of sepsis, including signs of lung consolidation or findings consistent with an acute abdomen. * Carefully examine sites of intravascular lines, surgical wounds, drain sites, and decubiti for evidence of infection. * Because cardiogenic pulmonary edema must be distinguished from ARDS, carefully look for signs of congestive heart failure or intravascular volume overload, including jugular venous distension, cardiac murmurs and gallops, hepatomegaly, and edema. Causes of ARDS * Risk factors for ARDS include direct lung injury, systemic illnesses, and injuries. * The most common risk factor for ARDS is sepsis. Other nonthoracic conditions contributing to the risk for developing ARDS include trauma with or without massive transfusion, acute pancreatitis, drug overdose, burns and long bone fracture. * The most common direct lung injury associated with ARDS is aspiration of gastric contents. * Other risk factors include various viral and bacterial pneumonias, near drowning, and toxic inhalations. * General risk factors for ARDS have not been prospectively studied using the 1994 EACC criteria. However, several factors appear to increase the risk of ARDS after an inciting event, including advanced age, female sex (noted only in trauma cases), cigarette smoking, and alcohol use. For any underlying cause, increasingly severe illness as predicted by a severity scoring system such as acute physiology and chronic health evaluation (APACHE) increases the risk of development of ARDS. Lab studies * In addition to hypoxemia, arterial blood gases often initially show a respiratory alkalosis. However, in ARDS occurring in the context of sepsis, a metabolic acidosis with or without respiratory compensation may be present. As the condition progresses and the work of breathing increases, the partial pressure of carbon dioxide (PCO2) begins to rise and respiratory alkalosis gives way to respiratory acidosis. * ARDS is a clinical diagnosis, and no specific laboratory abnormalities are noted beyond the expected disturbances in gas exchange and radiographic findings. ARDS is defined by a PaO2/FiO2 ratio of less than 200 and ALI by a ratio of less than 200. Other abnormalities observed depend on the underlying cause or associated complications and may include the following: * Hematologic: In septic patients, leukopenia or leukocytosis may be noted Thrombocytopenia may be observed in septic patients in the presence of disseminated intravascular coagulation (DIC). Von Willebrand factor (VWF) may be elevated in patients at risk for ARDS and may be a

Theres somethings that say not congestive heart failure, but we dont know (no cephalization, etc)

There is no typical physical exam.

Many things can cause ARDs

APACHE is mostly used to compare different populations of patients. (statistical)

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(DIC). Von Willebrand factor (VWF) may be elevated in patients at risk for ARDS and may be a marker of endothelial injury. * Renal: Acute tubular necrosis (ATN) often ensues in the course of ARDS, probably from ischemia to the kidneys. * Hepatic: Liver function abnormalities may be noted in either a pattern of hepatocellular injury or cholestasis. * Cytokines: Multiple cytokines, such as IL-1, IL-6, and IL-8, are elevated in the serum of patients at risk for ARDS.

Check liver enzymes because they usually bump out. They track the Cytokines, they are giong to be through the roooof!

PROCEDURES IN ARDS
PA catheters * Hemodynamic monitoring with pulmonary artery (Swan-Ganz) catheter * Because the differential diagnosis of ARDS includes cardiogenic pulmonary edema, hemodynamic monitoring with the Swan-Ganz catheter is often helpful in separating cardiogenic from noncardiogenic pulmonary edema. The pulmonary artery catheter is floated through an introducer that is placed in a central vein, usually the right internal jugular or subclavian vein. With the balloon inflated, the catheter is advanced with continuous pressure monitoring. Never advance with balloon down. This allows measurement of right atrial pressure, right ventricular pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure (PCWP). With the catheter properly positioned, the PCWP reflects filling pressures on the left side of the heart and, indirectly, intravascular volume status. A PCWP of less than 18 mm Hg is usually consistent with noncardiogenic pulmonary edema, although other factors, such as a low plasma oncotic pressure, may allow cardiogenic pulmonary edema to occur at lower pressures. FOB with BALl and Peanut Butter Biscuit. FOB with BAL and PBB * Bronchoscopy with Bronchoalveolar Lavage or Protected Brush Bx * Bronchoscopy should be done to evaluate the possibility of infection in patients acutely ill with bilateral pulmonary infiltrates. Culture material may be obtained by wedging the bronchoscope in a subsegmental bronchus and collecting the fluid suctioned after instilling large volumes of nonbacteriostatic saline (BAL). The fluid is analyzed for cell differential, cytology, silver stain, and Gram stain and is quantitatively cultured. * 10x3 CCU for Protected Brush Biopsy ( PBB) and 10x4 CCU for BAL. The presence of neutrophils in the lavage with intracellular organisms in these cells is also consistent with infection. * Analysis of the types of cells present in the BAL fluid may be helpful in the differential diagnosis of patients with ARDS. For example, the finding of a high percentage of eosinophils (>20%) in the BAL fluid is consistent with the diagnosis of acute eosinophilic pneumonia. The use of high-dose corticosteroids in these patients may be lifesaving. A high proportion of lymphocytes may be observed in acute hypersensitivity pneumonitis, sarcoidosis, or bronchiolitis obliteransorganizing pneumonia (BOOP). * Cytologic evaluation of the BAL fluid may also be helpful in the differential diagnosis of ARDS. This may reveal viral cytopathic changes for example. Silver stain may be helpful in diagnosing an infection, such as Pneumocystis. This is what one looks like. Bronchoscope procedure being doen outpatient Carina, trachial rings. These keep subdividing. Mechanical Ventilation * Positive end-expiratory pressure or continuous positive airway pressure * ARDS is characterized by severe hypoxemia. When oxygenation cannot be maintained despite high inspired oxygen concentrations, the use of CPAP or PEEP usually promotes improved oxygenation, allowing for tapering of the FIO2. * By maintaining the alveoli in an expanded state throughout the respiratory cycle, PEEP/CPAP may decrease shear forces that promote ventilator-associated lung injury. * The best method for finding the optimal level of PEEP/CPAP in patients with ARDS is controversial. * Increase in increments of 2-3 until able to decrease FIO2 below 65% if possible. If not, lowest FIO2 to keep PO2 above 50-55 PCV / IRV / IRPCV * Pressure-controlled ventilation and high frequency ventilation * If high inspiratory airway pressures are required to deliver even low tidal volumes, pressurecontrolled ventilation (PCV) may be initiated. In this mode of mechanical ventilation, the physician sets the level of pressure above PEEP/CPAP and the inspiratory time (I-time) or inspiratory/expiratory (I:E) ratio. The resultant tidal volume depends on lung compliance and increases as ARDS improves. If oxygenation is a problem, longer I-times, such that inspiration is longer than expiration (inverse I:E ratio ventilation) may be beneficial. Ratios as high as 4:1 can be used. * Evidence indicates that PCV may be beneficial in ARDS, even without the special circumstances noted. In a multicenter controlled trial comparing VCV to PCV in patients with ARDS, Esteban (2000) found that PCV resulted in fewer organ system failures and lower mortality rates than VCV, despite use of the same tidal volumes and peak inspiratory pressures. A larger trial is needed before a definite recommendation is made. Machine gives us the long inspiration, but we cant go above it, then look how little expiration time we have. That is the I,E ratio of 1.5:1. What happens to the PCO2 if you have longer inspiratory time? It goes up, permissive Permissive Hypercapnia hypercapnia. When we first started doing this stuff,t he pH just started dropping, professor * Hypoventilation with permitted hypercapnia used to get nervous at pH of 7.1-7.15 * Avoids high lung volume and pressure stretching * Hypercapnia may protect against lung and systemic organ injury * ???-acidosis protection, attenuated free radical formation, interference of cytokine signaling There is some questino about whether the permissive hypercania plays a protective role, It has * Buffering is common but controversial- permitted in ARDSnet study atenuated free radicals, and interference of cytokine signaling. But just know this is the result, and it may be protective. Jet and Liquid Ventilation * High frequency ventilation (jet or oscillatory) is a ventilator mode that uses low tidal volumes and high respiratory rates. With the knowledge that distension of alveoli is one of the mechanisms promoting ventilator-associated lung injury, high frequency ventilation would be expected to be beneficial in ARDS. Results of clinical trials in adults have generally demonstrated early improvement in oxygenation when compared with conventional ventilation but no improvement in survival. In the largest randomized controlled trial, 148 adults with ARDS were randomized to conventional ventilation or high frequency oscillatory ventilation (HFOV). The HFOV group had early improvement in oxygenation that did not persist beyond 24 hours. The 30-day mortality in the HFOV group was 37% compared with 52% in the conventional ventilation group, but this difference was not statistically significant (Derdak, 2002).

You put your scope down into the lung, you run the protected brush down into the lung, looks like a q tip, in and out a few times, pull it back out, clip it off and send it for culture, If it comes back with greater than 10 to the third of colony forming units, then something. If its greather than 10 to the 4th, then pretty much diagnostic.

Severe hypoxia with ARDs Higher levels of FiO2 higher levels of PEEP

Its muthafreakin cold up in here!!!

* Partial liquid ventilation has also been tried in ARDS and in a randomized controlled trial in which it was compared with conventional mechanical ventilation, resulted in increased morbidity (pneumothoraces, hypotensions, and hypoxemic episodes), and a trend toward higher mortality (Kacmarek, 2006). Prone Position

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* Although, 60-75% of patients with ARDS have significantly improved oxygenation when turned from the supine to the prone position, no survival benefit exists for patients treated in the prone position. When the prone position is used, the improvement in oxygenation is rapid and often significant enough to allow reductions in FIO2 or level of CPAP. The improvement in oxygenation may persist after the patient is returned to the supine position and may occur on repeat trials in patients who did not respond initially. * Possible mechanisms for the improvement noted are recruitment of dependent lung zones, increased functional residual capacity (FRC), improved diaphragmatic excursion, increased cardiac output, and improved ventilation-perfusion matching. Despite improved oxygenation with the prone position, randomized controlled trial of the prone position in ARDS have not demonstrated improved survival. Experimental Rxs * Nitric Oxide- reduces pulmonary vascular resistance * Surfactant- a dysfunction correction * NSAIDs- inhibit prostaglandin pathways * Prostaglandin E1- decreases inflammatory response * Steroids- ?????????????????????????? Steroids * Corticosteroids do not improve outcomes in acute respiratory distress syndrome (ARDS), and if started after 2 weeks, they may increase mortality, according to the results of a randomized study published in the April 20, 2006 issue of The New England Journal of Medicine. * "Persistent ARDS is characterized by excessive fibroproliferation, ongoing inflammation, prolonged mechanical ventilation, and a substantial risk of death," write Kenneth P. Steinberg, MD, from the University of Washington, Seattle, and colleagues from The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. "Because previous reports suggested that corticosteroids may improve survival, we performed a multicenter, randomized controlled trial of corticosteroids in patients with persistent ARDS. * In this double-blind study, 180 patients with ARDS of at least 7 days' duration were randomized to receive either methylprednisolone or placebo. The main outcome was mortality at 60 days, and secondary outcomes included the number of ventilator-free days and organ-failurefree days, biochemical markers of inflammation and fibroproliferation, and infectious complications. * Hospital mortality rate at 60 days was 28.6% in the placebo group (95% confidence interval [CI], 20.3% - 38.6%) and 29.2% in the methylprednisolone group (95% CI, 20.8 - 39.4%; P = 1.0). At 180 days, the rates were 31.9% (95% CI, 23.2% - 42.0%) and 31.5% (95% CI, 22.8% - 41.7%), respectively (P = 1.0). * Methylprednisolone Infusion in Early Severe ARDS*Results of a Randomized Controlled Trial * G. Umberto Meduri, MD, FCCP; Emmel Golden, MD; Amado X. Freire, MD, MPH, FCCP; Edwin Taylor, MD; Muhammad Zaman, MD; Stephanie J. Carson, RN; Mary Gibson, RN and Reba Umberger, RN, MS * * From the Memphis Lung Research Program (Dr. Meduri, Ms. Carson, Ms. Gibson, and Ms. Umberger), Baptist Memorial Hospital (Dr. Golden), Regional Medical Center (Dr. Freire), the Veterans Affairs Medical Center Memphis (Dr. Zaman), and St. Francis Hospital (Dr. Taylor), Memphis, TN.

* Objective: To determine the effects of low-dose prolonged methylprednisolone infusion on lung function in patients with early severe ARDS. * Design: Randomized, double-blind, placebo-controlled trial. * * Participants: Ninety-one patients with severe early ARDS ( 72 h), 66% with sepsis. * Interventions: Patients were randomized (2:1 fashion) to methylprednisolone infusion (1 mg/kg/d) vs placebo. The duration of treatment was up to 28 days. Infection surveillance and avoidance of paralysis were integral components of the protocol. * Main outcome measure: The predefined primary end point was a 1-point reduction in lung injury score (LIS) or successful extubation by day 7. * Results: In intention-to-treat analysis, the response of the two groups (63 treated and 28 control) clearly diverged by day 7, with twice the proportion of treated patients achieving a 1-point reduction in LIS (69.8% vs 35.7%; p = 0.002) and breathing without assistance (53.9% vs 25.0%; p = 0.01). Treated patients had significant reduction in C-reactive protein levels, and by day 7 had lower LIS and multiple organ dysfunction syndrome scores. Treatment was associated with a reduction in the duration of mechanical ventilation (p = 0.002), ICU stay (p = 0.007), and ICU mortality (20.6% vs 42.9%; p = 0.03). Treated patients had a lower rate of infections (p = 0.0002), and infection surveillance identified 56% of nosocomial infections in patients without fever. * Conclusions: Methylprednisolone-induced down-regulation of systemic inflammation was associated with significant improvement in pulmonary and extrapulmonary organ dysfunction and reduction in duration of mechanical ventilation and ICU length of stay.

Shock:
A momentary pause in the act of death. -John Collins Warren, 1800s Definition SHOCK: syndrome of inadequate organ perfusion to meet the tissues oxygenation demand SHOCK SYNDROME * Shock is a condition in which the cardiovascular system fails to perfuse tissues adequately * An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues * Inadequate tissue perfusion can result in: * generalized cellular hypoxia (starvation) * widespread impairment of cellular metabolism * tissue damage * organ failure * death PATHOPHYSIOLOGY OF SHOCK SYNDROME * Impaired tissue perfusion : imbalance between cellular oxygen supply + cellular oxygen demand * All Types of shock eventually result in impaired tissue perfusion & the development of acute circulatory failure or shock syndrome

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circulatory failure or shock syndrome PATHOPHYSIOLOGY OF SHOCK SYNDROME Cells switch from aerobic --> anaerobic metabolism lactic acid production Cell function ceases & swells membrane becomes more permeable electrolytes & fluids seep in & out of cell Na+/K+ pump impaired mitochondria damage cell death

COMPENSATORY MECHANISMS: 1. Sympathetic Nervous System Stimulated by baro-receptors: * Increased heart rate * Increased contractility * Vasoconstriction (SVR -->Afterload) * Increased Preload COMPENSATORY MECHANISMS: 2.Renin-angiotension system * Decrease renal perfusion --> * Releases Renin : Angiotensinogen --> Angiotesin I * Angiotesin I --> Angiotensin II * Vasoconstriction * Releases aldosterone adrenal cortex * Sodium & water retention COMPENSATORY MECHANISMS 3. Antidiuretic Hormone * Osmoreceptors - hypothalamus * ADH - Posterior pituitary gland * Vasopressor effect to increase BP * Acts on renal tubules to retain water COMPENSATORY MECHANISMS 4. ACTH * Anterior pituitary --> ACTH * Stimulates adrenal cortex --> glucorticoids * Blood sugar to meet increased metabolic needs Pathophysiology - Systemic Level * Systemic lactic acidosis * Myocardial contractility * Vascular tone * blood pressure --> preload --> cardiac output Shock is a symptom of its cause. Clinical Presentation: Generalized Shock * Vital signs * Hypotensive :(may be WNL / due to compensatory mechanism) < 90 mmHg / 40 mmHg from baseline * MAP < 60 mmHg * Tachycardia: Weak and Thready pulse * Tachypneic blow off CO2 Respiratory alkalosis Clinical Presentation: Generalized Shock * Mental status: * restless * Irritable + apprehensive * unresponsive * LOC * Urine output Shock Syndromes * Hypovolemic Shock * blood VOLUME problem * Cardiogenic & Obstructive Shock * blood PUMP problem * Distributive Shock [septic / anaphylactic / neurogenic] * blood VESSEL problem Why Monitor? * Essential to understanding the disease * Describe the patients physiologic status * Facilitates diagnosis + treatment of shock Recall the 4 major determinants of cardiac function * Preload * Afterload * Heart rate * Contractility Frank Starling Principle * CO LVEDV * SV RAP * Cardiac output is directly related to venous return Pulmonary Artery Catheter Pulmonary Artery Catheter - PAC * INDICATIONS * volume status * cardiac status * COMPLICATIONS * technical * anatomic * physiologic

Protective mechanisms sometimes work against you.

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Correct PAC Position Wrong location, went too far They can knot up, one of the complications. Complications * PTX: 2% to 4%- depends on route * Arrhythmias: RBBB 5% * Knotting: ? * PA perforation: < 1% * Infection: 1% per day * Pulmonary Infarction: < 7% Standard Parameters * Measured * Blood pressure * Pulmonary A. pressure * Heart rate * Cardiac Output * Stroke volume * Wedge pressure * CVP * Calculated * Mean BP * Mean PAP * Cardiac Index * Stroke volume index * SVRI * LVSWI * BSA Why Index? * Body habitus + size is individual * Inter-patient variability does not allow normal ranges * Indexing to patient with BSA allows for reproducible standard Index Example PATIENT A * 60 yo male * 50 kg * CO = 4.0 L/min * BSA = 1.86 CI = 2.4 L/min/m2 PATIENT B * 60 yo male * 150 kg * CO = 4.0 L/min * BSA = 2.64 CI = 1.5 L/min/m2 PA Insertion CVP ~ right atrial pressure ~ right ventricular end diastolic volume (preload ) * CVP of SGC at level of right atrium * pre-load assessment * normal 5-10 mm Hg * limited value * Increase CVP * * * * * * * * * * * * * * High Intravascular Volume Renal Failure Pulmonary Hypertension Vasoconstriction Vasopressors Hypothermia High PEEP due to increase in intrathoracic pressure Decrease CVP Hypovolemia Pooling of blood in extremity or gut Hyperthermia 3rd Spacing Septic Shock Arrhythmias

PAOP(PCWP) =~ LAP =~ LVEDP * End expiration * Reflection changes with positive pressure ventilation * Waveforms change every 20 cm * 6 15 mm Hg PAOP(PCWP) * Indirect indicator of left ventricular filling pressure or preload. MONEY SLIDE!

* When the balloon of the PA catheter is inflated, a branch of the pulmonary artery is occluded. * The pressure that is transmitted by the pulmonary vein is approximately the same as the lead atrial pressure because there are no valves is the lung vasculature that would create a change in pressure between the left ventricle and the pulmonary vein Increase in PCWP * Intravascular Volume Overload * Mitral Valve Stenosis * Left Ventricular Failure * Cardiogenic Shock High * PEEP (to estimate PCWP when pt. is on PEEP: PCWP - 1/2PEEP = corrected PCWP) Decrease in PCWP * Hypovolemia * Right Ventricular Infarction Some of the things we calculate. Just for us, not for the test. Hemodynamic Calculations Cardiac Index C.I. = HR x SI SI : stroke index measures, the amount of blood ejected by the ventricle with each cardiac contraction

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SI : stroke index measures, the amount of blood ejected by the ventricle with each cardiac contraction Total peripheral resistance (SVRI) * SVR (Systemic Vascular Resistance) measures the afterload or resistance applied to the left ventricle. * It is an indicator of the left ventricular afterload. It is the force impeding the ejection of blood from the left ventricle. * Normal: 800-1200dynes/sec/cm2 * vasoconstrictio * vasodilation

* Increase in SVR * * * * * * * Hypoperfusion Hypovolemia Hypothermia Use of Vasopressors/Inotropes Cardiogenic Shock Left Ventricular Failure Decrease SVR Just common sense stuff. Know the numbers about ARDs and Pulmonary Capillary Wedge pressure

* Sepsis Anaphylaxis Reaction * Hyperthermia * Vasodilators PVR (Pulmonary Vascular Resistance) * Measures the resistance or impedance of blood flow from the right ventricle against the pulmonary circulation. * It measures resistance across the entire lung field. * Normal: 150-250dynes/sec/cm5 * Increase PVR * CHF * Pulmonary Hypertension * Pulmonary Edema * ARDS * Hypoxia * Pulmonary Emboli Too Many Numbers Oxygen Calculations * Arterial Oxygen Content (CaO2) * Venous Oxygen Content (CvO2) * Arteriovenous Oxygen Difference (avDO2) * Delivery (O2AVI) / (DO2I) * Consumption (VO2I) Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption Oxygen * O2 Delivery - volume of gaseous O2 delivered to the LV/min. * O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min. * O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner Arterial Oxygen Content Is the actual amount of oxygen found bound to hemoglobin and dissolved in the plasma in each l00cc of arterial blood. CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031) Normal: 17-20ml/dl

* Decrease in Ca02 * Decreased Hgb levels * ARDS * Pulmonary Emboli * Pneumonia * Pulmonary Edema * Hypoxia Classification of Shock Type PAOP C.O. HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE or N varies

SVR

OBSTRUCTIVE SIRS - Distributive Shock * Prompt volume replacement - fill the tank * Early antibiotic administration - treat the cause * Inotropes - first try Dopamine * If MAP < 60 * Dopamine = 2 - 3 mg/kg/min * Norepinephrine = titrate (1-100 mg/min) * R/O missed injury Vasopressor Agents * Augments contractility * after preload established * thus improving cardiac output * Risk tachycardia + increased myocardial oxygen consumption if used too soon * Rationale increased C.I. improves global perfusion Dopamine * Low dose (0.5 - 2 mg/kg/min) = dopaminergic * Moderate dose (3-10 mg/kg/min) = b-effects * High dose (> 10 mg/kg/min) = a-effects * SIDE EFFECTS * tachycardia * > 20 mg/kg/min D to norepinephrine Dobutamine

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Dobutamine -agonist * 5 - 20 mg/kg/min * potent inotrope * variable chronotrope * caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension Norepinephrine * Potent a-adrenergic vasopressor * Some b-adrenergic, inotropic, chronotropic * Dose 1 - 100 mg/min * Unproven effect with low-dose dopamine to protect renal and mesenteric flow Epinephrine - and b-adrenergic effects * potent inotrope and chronotrope * dose 1 - 10 mg/min * increases myocardial oxygen consumption particularly in coronary heart disease Amrinone * Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects * increased cardiac stroke output without an increase in cardiac stroke work * most often added with dobutamine as a second agent * load dose = 0.75 -1.5 mg/kg 5 - 10 mg/kg/min drip * main side-effect - thrombocytopenia Anaphylaxis * Epinephrine 0.2-0.5 mL SC of 1:1000 * Diphenhydramine 50-80 mg IM / IV - urticaria / angioedema * Inhaled bronchodilators / intravenous aminophylline - bronchospasm

ANTIBIOTICS Surgical Care * Remove: infected catheters / prosthesis +foreign bodies * Drain: intra-abdominal abscess, postoperative collections, soft tissue abscess, and gallbladder * Debridement of devitalized tissue: pancreatic necrosi +soft tissue infections * Operative resection : inflamed, infarcted, ischemic, and perforated hollow viscus * Amputation of gangrenous extremities No source evident in a healthy host * Third-generation cephalosporin * Ceftriaxone 2 g IV q12h * Ceftizoxime * Ceftazidime In a healthy host * Nafcillin + aminoglycoside * Imipenem, piperacillin / tazobactam No source evident in an immunocompromised host * Ceftazidime 2 g IV q8h * + Aminoglycoside * Imipenem / piperacillin / tazobactam * + Aminoglycoside No source evident in a user of intravenous drugs * Nafcillin 2 g IV q4h * + Aminoglycoside * Vancomycin + aminoglycoside, * Ceftazidime * Imipenem * Piperacillin / tazobactam

Bacterial pneumonia, hospital acquired * Ceftazidime 2 g IV q8h * + Aminoglycoside * + Macrolide * Imipenem * Piperacillin / tazobactam + aminoglycoside + macrolide

Urinary tract infection * Ampicillin 2 g IV q4h * + Aminoglycoside * Fluoroquinolone * Third-generation cephalosporin + aminoglycoside Mixed aerobic + anaerobic abdominal sepsis, aspiration pneumonia, pelvic infection, and necrotizing cellulitis * Third-generation cephalosporin / Ampicillin 2 g IV q4h * + Aminoglycoside * + Clindamycin 600 mg IV q8h / metronidazole 500 mg IV q6h * Fluoroquinolone + clindamycin * Imipenem * Piperacillin / tazobactam

Meningitis * Ceftriaxone 2 g IV q12h * + Vancomycin * Meropenem + vancomycin * chloramphenicol + cotrimoxazole + vancomycin

Cellulitis / Erysipelas * Nafcillin 2 g IV q4h * Cefazolin * Vancomycin * Clindamycin What is ARDS , how do you treat shock 2,3 questions

TSS / Streptococcal necrotizing fascitis * Pen G 8-10 million Us IV q4-6h * 1 gen. Cephalosporin

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* 1 gen. Cephalosporin * Vancomycin * Nafcillin

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