SCARED Stanford Course on Active Resuscitation, Evaluation, and Decision making 2005 Geoff Lighthhall MD, PhD Assistant Professor, Anesthesia and Critical Care Stanford University School of Medicine Course Faculty: Geoff Lighthall MD, PhD T. Kyle Harrison MD Department of Anesthesia Stanford University School of Medicine and VA Palo Alto Patient Safety Center of Inquiry 1 SCARED Introductory Material: Epidemiology and physiology of patients that experience cardiopulmonary arrest 3. 5. Introduction to the course Medical illness, the golden hour, and missed opportunities to prevent cardiopulmonary arrest Evaluation and Stabilization of Critically Ill Patients Recognition and resuscitation of unstable patients 12. 14. 20. 22. 25. 28. 31. 33. 34. 38. Immediate assessment and stabilization Respiratory failure: Physiology of respiration and gas exchange Stabilization and therapy for respiratory problems Physiology of oxygen transport abnormalities Circulatory Shock & Hypotension Therapy for hemodynamic instability Acute blood loss and massive transfusion Acute pain Leadership in medical emergencies References 2 I. Technical skills for early resuscitation Why bother spending another nice evening in the hospital? In short, we want to leave you confident and ready to tackle the problems of the hospital's sickest patients, and to start thinking how you may function better as a member or leader of a resuscitation team. This is an important area that is generally neglected in medical training, yet in a perfect system, should be the one that receives extra attention. The drive to offer this course came from discussions and questionnaire responses from the VA ICU simulator course where participants voiced an interest receiving additional training in managing emergencies and cardiac arrests--and specifically, the technical aspects of such care. The types of emergencies you will be called to manage can be crudely classified as cardiac arrests—the four prototypic ACLS emergencies—and pre arrests. While good skills in managing code patients is important, we also recognize that even with the best team and effort, a meaningful survival is rare. Since most cardiac arrests result from medical problems that if corrected, offer a much better potential for survival, and since such problems persist for a while before becoming “arrests,” proper management of the pre-arrests is crucial. Indeed, improving the care of the latter set of patients has provided a great deal of motivation worldwide for the development of medical emergency teams, and personal motivation for offering this course. The patients you will manage in this course may have conditions that degenerate to cardiac arrest. So while we will provide experience with some code situations, also think about how tragedy can be averted before the onset of cardiopulmonary arrest. By the conclusion of this session, you will hopefully have some fear for the patients who require emergent help as well as the sense that you have more to offer. Goals Provide mentorship and training in specific critical events using both short discussions and hands-on experience with human patient simulation. Take what you already know about the pathophysiology of critical illness, cardiac instability, and ACLS, and repackage that knowledge in a system that might be of greater utility. Focus on your role and responsibilities as a team leader Provide some check lists and hand cards that can be of use in a real emergency. Give you some guidelines and pointers on drug dosing and kinetics that you can use in your practice 3 Overall Philosophy The ability to prevent further decompensation and codes depends upon how clearly you understand the nature of a patient’s problem and the need to correct it. We focus on the issues of respiration and tissue oxygen delivery as the common origin of most emergencies that result in “codes.” Our approach is to analyze the physiologic roots of cardiovascular and respiratory problems, and use this knowledge as a guide toward earlier early empiric therapy, and hopefully rapid treatment of unstable patients. This approach is apparent in the cards or “cognitive aids” that we have made. Cognitive Aids There is plenty of scientific evidence that people under stress function at a small fraction of their overall mental capacity. Somehow, medicine has confused patient safety and administration of acute care with performance art, and has been reluctant to accept the idea of its practitioners using cards, cheat sheets, phone calls, or other reference material when lives are at risk. There is no weakness in using such materials in managing a stressful situation. Once you accept this view, you will be far more useful and reliable in emergencies. For this course, we have made a great effort in assembling information in a relevant format for your use in emergencies. The cognitive aids you will receive have been developed by the course instructors who have extensive experience studying how others manage emergencies, how physicians behave under such stress, what kinds of information physicians need to manage emergencies, and what type materials currently in use work and don’t work. The cognitive aids here come in a few flavors: Simplified ACLS algorithms Physiologic roots of key hemodynamic and respiratory problems Check lists for airway, breathing and circulatory emergencies (A, B & C cards) A card that describes emergency management in general Each type of generic problem (hypotension, shock, hypercarbia and hypoxemia), is pulled apart into its various components with possible causes for each noted. Using the shock/ hypotension card as an example, the physiologic roots of low Blood pressure and low oxygen delivery are noted in black; “data” that one may gather from monitors, lab studies and physical exam, are noted in red; and likely diagnoses are in blue. By walking down a physiologic tree and using available data to sort out which branches are more likely, one arrives at a set of provisional diagnoses as well as the nature of the problem to be corrected (low SVR, for example). If insufficient data is available, the information on the card may also point out to you what additional studies or findings may be of greatest yield or utility. Additionally, there is also a section on what the team leader should be doing for each emergency. 4 II. Background. Medical illness, the golden hour, and missed opportunities to prevent cardiopulmonary arrest In some disease entities such as major pulmonary embolus, myocardial infarction, stroke and trauma, the benefits of early stabilization and treatment are well-known. However, the extent to which survival from other forms of clinical instability can be enhanced by rapid intervention has not been defined. Even with reasonable face validity, this concept remains under-appreciated. The educational mission of a teaching hospital may create some delays in care that are deleterious. In most residency programs, interns and senior medical students are given the responsibility as primary caretaker for hospitalized patients. Despite the presence of more experienced fellows, residents and attendings on the care team, tradition dictates that the team be contacted through the intern or resident when a patient’s condition changes. During night hours, the primary team in charge of a patient is rarely intact, with some form of cross-coverage system (typically consisting of mid level resident) in charge of emergency calls. Compliance with resident work hour restrictions requires even greater reliance on shift care or cross-coverage schemes where there is greater likelihood that physicians will be called about patients for whom they have little familiarity. Overall, unless a diagnosis is immediately clear, valuable time can be spent on an intern’s initial evaluation, subsequent resident evaluation and further evaluation by other consultants before stabilization and definitive therapy are initiated. The overall strength of the current system has not been directly tested. For example for every 1000 ward admissions, we have no idea how may of these patients show signs of instability that result in calls to the house staff with a subsequent evaluation or decision-making that corrects the patient’s course without resulting in an ICU admission,cardiac arrest, or death. However, by analyzing the converse--the natural histories of patients whose course does result in death, cardiac arrest, or ICU admission--we do have a data set that is quite revealing. Antecedents to Intensive Care Unit admission Patents admitted to an ICU from an impatient ward have a higher mortality than those from other hospital locations (2). Studies evaluating patterns of ward care prior to ICU admission show a general lack of time urgency in evaluating and treating patients with abnormal vital signs and other forms of deterioration (35) . With appropriate adjustments for co-morbidities and disease severity, patients initially admitted to hospital wards (as opposed to ICU) had up to a fourfold increase risk of mortality, suggesting that the nature of the care was a more significant determinant of ultimate clinical trajectory than the admitting diagnosis (3). Deterioration in the admitting condition or the development of new problems were key risks for a worse outcome (3). In another study, a different group investigators had experts rate the quality of care provided to patients admitted to the intensive care unit (6). Care 5 was rated as either “well managed,” or “deficient,” or “equivocal” if the raters could not agree. The group of patients considered to have suboptimal care had twice the ICU mortality rate of the other groups. Areas considered problematic were: timing of admission (late), and management of oxygen therapy, airway, breathing, circulation, and monitoring (6). Reasons for underlying suboptimal care were “failure or organization, lack of knowledge, failure to appreciate clinical urgency, lack of experience, supervision, and failure to seek advice.” Our own experience in examining dynamic decision making of house staff in a fully simulated ICU revealed similar classes of deficiencies, including non-adherence to established protocols (7). In reviewing studies of the pre-ICU phase of patient care, it is attractive to think that all problems would be solved solely by earlier admission or transfer to a higher level of care. This is not always practical in situations where ICU beds may be in short supply. Even when ICU beds are abundant, a number of personal and professional barriers may prevent clinicians from admitting patients with real but non-catastrophic abnormalities. These barriers can be summarized as follows: A lack of familiarity with the ICU that may prevent some from considering transfer to this setting (17). A mentality that tends to block admissions to patients unless they need mechanical ventilation, invasive lines, or other high-order intervention. The mentality generally ignores the type of patients that are the most likely to gain the greatest yield from intensive care resources. A vague sense of personal failure that comes from admitting a patient to the ICU, and a sense of pride that comes from preventing an ICU admission. A related sense of personal duty to try to do everything for the patient before admitting that there are forces you cannot control. A general reluctance to ask for help or sense that you shouldn’t. Competing educational missions that prevent one from wanting to give up a “good teaching case.” All of the above PLUS lack of involvement of attending physicians. Antecedents to cardiac arrest calls Cardiac arrest is not only the result of cardiac decompensation, but the final common pathway for all lethal disease processes that go uncorrected. The potential for survival is largely lost at the time of cardiopulmonary arrest. In one study covering over 12,000 admissions to intensive care units in the UK, 33% of all mortality followed cardiopulmonary resuscitation (2). Other large series of cardiac arrests show an initial resuscitation rate of 25-40%, but subsequent ICU, and hospital survival rates that drop sharply to the range of 10-15%, with even fewer making a full neurologic recovery (5, 8, 9). Patients admitted to the ICU following cardiac arrest have allowed retrospective analysis of factors presaging their decompensation. Two different studies of antecedents to cardiac arrest demonstrated that between 75%- 85% of the affected patients had some form of deterioration in the hours prior to the 6 arrest (4, 10). Nearly a third of such abnormalities persisted for greater than 24 hours prior to arrest, with a population mean of 6.5 hours (4). In Schein’s series, the vast majority (76%) of the disease processes eventually progressing to cardiac arrest were not considered to be intrinsically rapidly fatal. In yet another series over half of the arrests presented ample warning of decompensation: the majority had uncorrected hypotension, and half of these had systolic blood pressures less than 80mm Hg for more than 24 hours. Others had severe, but correctable abnormalities such as hypokalemia, hypoglycemia and hypoxemia (11). The collective experience suggests that the quality of care, more than the disease may be responsible for the poor immediate survival of these patients. Inattention to, or unawareness of a developing serious problem causes the additional problem of hasty decision making at the time of cardiac arrest. Once a cardiac arrest has occurred, the clinicians hand is forced and ICU admission becomes mandatory. Why does this poor care preceding cardiac arrest occur? Problems with establishing proper care were found to exist at multiple levels: nurses were not calling physicians for patients with abnormal vital signs or changes in sensorum; physicians did not fully evaluate abnormalities when they were contacted; ICU consultants were not called in routinely, and even senior level or consulting ICU caregivers did not obtain routine studies such as blood gasses, hematocrits and electrolyte studies that would have defined the patient’s problem. In cases when laboratory studies were done, they were not always interpreted correctly, and when they were, therapy was not always initiated (5). The pattern is shown graphically to demonstrate that the timely pairing between an abnormality and therapy--the reason to have someone hospitalized---does not occur. A continuum exists between common physiologic abnormalities and their deterioration into a code. Thus while you cannot be a ‘little bit’ pregnant, you can have a ‘little bit’ of VT, VF, pulseless electrical activity and asystole. 7 The ideal situation for a patient would be one in which a problem requiring treatment would manifest itself as some type of abnormality that would be recognized and acted upon in a tolerable amount of time. Given that this is a multi-step process in hospitals, the best analogy for a successful intervention would be a series of dominoes aligned such that triggering one is sure to activate the whole cascade in a predictable manner. What seems to be the case, however, is the existence of a series of roadblocks that allow only a certain percentage of traffic on to the next. The efficiency of throughput is highly variable, and is dependent on individual behavior and skill, cultural factors and other constraints. Common denominators amongst critical events In this case, critical event consists of either a code or an unplanned ICU admission--events that have been quantified in the literature that can be traced to underlying conditions or prior care as was done in the sections above. Looking at the literature as a whole, what stands out is the precarious nature of patients with the conditions listed below: 8 Conditions underlying critical events (given as a percentage of patients studied): Condition Tachypnea Hypotension Tachycardia GI bleed Cardiac/ MI Death 3,20 8-15 19-27 4-10 n/d Unplanned ICU admission15 Readmitted to ICU 15 Cardiac arrest 10 20-50 10-15 8 15 37 10-25 10-30 15 12 Multiple 30-45 26 The bottom line seems to be that respiratory insufficiency, hypotension, and tachycardia, along with depressed or altered mentation (not shown) are key findings that define patient deterioration in the pre-code stage. As far as things go, this is also fairly easy to catch. The vast majority of such abnormalities were present for hours prior to the “critical event.” That is not to say that all such abnormalities warrant ICU admission, but they do warrant a real evaluation and stabilization at a time when survival is possible (now), rather than later when survival is poor. III. The experience with early response teams Early response teams, or medical emergency teams (METs) were created with the goal is of improving the care and outcome of acutely worsening inpatients. The concept was an outgrowth of the work done in Australia and cited above, documenting the poor care preceding critical events. The common theme amongst hospitals instituting response teams is the creation of clear criteria for calling the team for a patient evaluation (see below). (12, 13, 19). Teams are mostly composed of senior ICU nurses in the UK, and senior residents and clinical fellows in Australia. Criteria for Calling VA Palo Alto Emergency Team (e Team) Airway Respiratory distress Threatened airway Breathing Resp rate > 30/ min Resp rate < 6/ min SaO2 < 90% on oxygen Difficulty speaking Circulation Systolic BP < 90 mm Hg despite treatment Pulse > 115/ min Neurology Any unexplained decrease in consciousness New onset of agitation or delerium Repeated or prolonged seizures Other Concern about patient Uncontrolled pain Failure to respond to treatments Unable to obtain prompt help or assistance 9 In non-academic centers, a crisis nurse and respiratory therapist constitute the team. At the University of Pittsburgh, the “medical emergency team” has the same members as the cardiac arrest team, but is paged in a slightly different manner. At the start of the 2005-2006 academic year, a medical emergency team will begin operation at VA Palo Alto (the “e Team”). Criteria for calling the e Team are listed above. Evaluation and efficacy of early response teams The impact of these teams has been evaluated by retrospective, concurrent, and multi-institutional models. In one UK hospital, vital status criteria such as those above were distributed and it became compulsory to contact the primary caregiver if any were present. A medical response team consisting of senior registrars (PGY 3-5 equivalents) and ICU nurses was created, but was not required to become involved in the care unstable patients unless requested by the primary caregiver. Compared to patients not attended to by the emergency team, the authors found significant decreases in cardiac arrests and ICU mortality rate (14). In Australia, the impact of an emergency response team instituted in one hospital was compared to two other hospitals that had traditional cardiac arrest teams (13). An increase in rates of new DNR orders and a decrease in mortality in patients with full code status was attributed to the team’s operation. In another Australian study, Buist described a program that led to significant decreases in cardiac arrests, hospital mortality and ICU death (19). Some believe that the success of the latter study is attributable to an increase in the diversion of terminally ill patients to a palliative mode of care rather than allowing the usual course of cardiopulmonary resuscitation, ICU admission and death. If so, this still constitutes a meaningful intervention that promotes patient comfort, minimizes distress, and conserves valuable resources. The other value of an ICU-based care team is the follow up of patients recently discharged from intensive care. As a population, former ICU patients have a two-fold higher rate of cardiac arrest than other ward patients (5), and a four to eleven-fold increase in the risk of in hospital death (15, 8). A primarily nurse-staffed team that followed post-ICU discharges was associated with an increased likelihood or survival to hospital discharge, and a significant decrease in ICU readmission (12). A study by Leary, however, did not find confirm that a medical response team changed the rate of readmission (16). 10 Summary of Rapid Medical Response Teams Described in the Literature Study author Mortality Cardiac arrest Buist, 200219 Decreased 2.5% Decreased 50% Ball, 200312 Decrease 6.8% Decrease 6.4% readmissions NO decrease in readmissions 17% decrease Decreased incidence Unchanged Decr. (RRR 65%) Leary, 200316 DeVita, 2004 Goldhill, 199914 Bristow, 200013 Bellomo, 2003 Bellomo, 2004** Ball. Leary Bellomo * Unchanged Decr. (RRR 26%) Decr. 37% ICU admission Morbidity/ LOS DNR orders Increased Decreased incidence Decreased (control OR 1.24-2.16) 80% Decr* Decr. In organ failures (range 57-88%) Decr. Mean LOS 4 days Examination of patients post ICU discharge Examination of patients post ICU discharge ICU beds occupied by cardiac arrest survivors ** postoperative patients Summary; the prognosis of deteriorating patients Disease processes with a reasonable survival are being converted to low survival processes such as cardiac arrest and multi-organ failure. Some patients are not appropriate for resuscitation. Survival of cardiac arrest victims is uniformly poor, yet a fair number end up in intensive care units and don’t do well even after staying there for prolonged periods of time. With warning signs present, many caregivers feel little pressure to act on abnormalities, yet failing to do so may result in a higher pressure situation (arrest), where decision making may be flawed, and where errors may occur more frequently. Establishment of a medical emergency/ early response teams have provided a heterogeneous array of benefits including improved survival, and prevention of futile resuscitation. Establishing such a team requires a commitment on an institution and its members to acknowledge shortcomings and weaknesses in the current system, and to reorganize responsibilities and priorities in a manner that is more likely to improve patient survival and hospital resource use 11 Immediate Assessment and Stabilization The overall emphasis of this course and its training exercises is to understand the physiology of deteriorating patients and think of problems, therapy, and end points in these terms. While subtle, this represents a departure from how most branches of medicine operate: “make a diagnosis then treat the problem.” The lack of a clear diagnosis seems to cause a bit of mental paralysis during the first 10-15 minutes of a critical patient encounter and this is exactly when initiating therapy is likely to have the greatest impact. A physiologic approach to patient care allows one to work with broad categories of problems and find diagnoses within this framework. More significantly, one gains the ability to start treatment for that class of problems at an earlier stage. This chapter will serve provide a general overview of patient resuscitation as a lead in to more detailed chapters on therapy for airway, breathing and circulatory disorders. An example You are called to evaluate a patient who is hypotensive. You arrive and find a patient with intact mental function, but with a BP of 85/49. The patient is warm to the touch and pulses are full. The patient has a respiratory rate of 24 with clear breath sounds; the chest seems to move with each heartbeat. From this brief exam, you can be fairly sure that the patient has no problem with cardiac function or with breathing. The extremities are warm, so you rule out an increase in vascular tone that one may expect if is the patient's hypotension was due to bleeding. Instead, you attribute the hypotension to vasodilation. Now you’re not quite sure whether the problem is sepsis due to cellulitis (the admitting condition), or due to an anaphylactic reaction associated with a recent antibiotic. Either way, you know that in a hypotensive patient with low SVR, administration of fluids and vasopressors is the mainstay of therapy. Better IV access is obtained, 50 mg of diphenhydramine and 2L of a crystalloid solution are quickly administered. The blood pressure improves with several 100mcg boluses of phenylephrine, during which time more fluids are given. Later, when the patient is more stable, you look up anaphylaxis and are reminded that a tryptase level would confirm this diagnosis, and a serum sample is sent. In this case, establishing a definitive diagnosis (worsening sepsis) lagged a few hours behind supportive therapy, but at least knowing the nature of the physiologic problem prevented time wasted on diagnostic studies, and facilitated early stabilization and probably a better clinical result. Caring for an unstable patient can be unnerving without some ability to prioritize problems. In the initial stages of any resuscitation, the focus is on cardiovascular and respiratory function and the absolute necessity of oxygen assimilation and delivery to the tissues in order to sustain life. The initial interventions are therefore: address the ABCs, collect and assess vital signs, assess the components of oxygen delivery. 12 Without a handle on these three basic points, it is unbelievably easy to get distracted with secondary phenomena and to waste crucial time on insignificant problems. While defining an unstable patient's problem in physiologic terms, it is important to also consider diagnoses that require external personnel or interventions as early as possible ( ie cardiac cath lab, surgical operation, special procedure); if in doubt, call for help at a stage when it can be useful. A more deliberate algorithm describing these priorities is summarized below, as well as a comparison of the ABCD survey taught in advanced cardiac life support (ACLS) courses. With cardiac arrest, survival correlates with conditions (heart rhythms) amenable to rapid correction by cardioversion, and accordingly, a high priority is assigned to identifying "shockable rhythms." Likewise, understanding the problem underlying the instability (ventricular tachycardia, pulseless electrical activity) will help you prevent a second code. In the absence of an emergency requiring defibrillation, the ACLS ABCD survey doesn’t provide any insight or guidance into the assessment and management of unstable patients, rather it suggests you establish a diagnosis for the instability. A preferable method is one that encompasses the overall issues of tissue oxygen delivery as it relates to cardiovascular and respiratory status, and one that allows for diagnosis and stabilization of both “coding” and “non-coding” patients. It is ABC VDE. As with any patient evaluation, a thorough physical exam should be performed at the earliest opportunity. Additional help may be needed to examine the patient, review the chart or computer, and to keep abreast of acute changes. A B C V D E This scheme -Airway -Breathing -Circulation -Vital signs--obtain -DO2—assess with ABG -Endocrine (check glucose) ACLS Primary Survey -Airway -Breathing -Circulation ACLS secondary 20 -Airway -Breathing -Circulation -Defibrillation -Diagnosis Why incorporate vital signs into a treatment algorithm? Isn't getting a set of vitals automatic??? Apparently not. Observations in real emergencies and in simulated emergencies repeatedly show clinicians standing around and failing to gather real time data, or relying on vital sign data in an unstable patient without knowing when it was obtained. The sections below will describe the function, assessment, and stabilization of abnormal breathing and circulation, and provide a detailed description of their evaluation. 13 Respiratory Failure: Physiologic and Anatomic Considerations Respiratory failure is a general term referring to impairment of the body’s ability to assimilate oxygen and transport it to the pulmonary capillary blood, eliminate carbon dioxide from the blood, or both. Organ-based derangements underlying such problems are diverse and include metabolic disturbances, dysfunction of neural circuitry from the brainstem down to the neuromuscular junction, abnormalities in the chest wall, alveoli, pulmonary parenchyma, upper and lower airways, and blood flow to the lung. In respiratory failure, diagnosis and intervention occur simultaneously, with support being the higher priority. Inspection and auscultation of the patient may provide enough information to initiate therapy, however, knowing whether the problem had a fast or slow onset will provide diagnostic information (i.e. was there a medicine recently given, was the patient eating, ambulating, etc). Respiratory failure usually involves an interplay between a disease process and host factors, all of which need to be considered as part of a management strategy. Most patients can tolerate an increased demand on the respiratory system for a few hours, some less. When a high workload is sustained, many patients experience respiratory muscle fatigue, and regardless of the inciting event, develop hypercapnic respiratory failure. When evaluating the patient, consider subjective complaints of fatigue and distress, and form your own impression of the work requirements of respiration. A more formal way to think of the patient’s work of breathing is in terms of the pulmonary compliance curve on the following page. The normal set point is in the center of the steep slope (FRC); thus little work (P, extravascular lung water, airway obstruction, or increased body girth function at a lower portion of the pulmonary compliance curve that requires far greater work for a given tidal volume (thick arrow). Patients with abnormal lung compliance also tend to breathe in a rapid shallow pattern; the resulting lower tidal volumes provide less efficient alveolar ventilation. The need for airway or ventilatory support as well as inquiry into code status is a prime consideration during the first seconds of an encounter. Supplemental oxygen should be given. A more detailed guide to the ABC survey is presented in the table below. Initiation of continuous oximetery and inspection of patient color provide immediate clues to whether the problem involves hypoxemia or not. Lastly, a blood gas will provide further assessment of gas exchange, CO2 elimination, and status of global oxygen delivery. 14 Compliance, C = V/ P Volume Inspiratory Pressure Airway: Look Can the patient talk, is there misting on mask? Chest rising? Abdominal retractions w/o chest rise? Listen Stethoscope to larynx: is there air movement? Stridor? Auscultation of chest Feel Can you feel breath on your hand? Chest rise Breathing: Look Patient color, speaking with complete sentences? Muscular movement Frequency, prolonged expiratory phase Chest rise, depth of respiration Does assist bag refill Listen Adventitious sounds; Diffuse? Focal? Bilateral air entry Feel Feel compliance of breathing circuit Feel chest rise Circulation: Look Color, capillary refill Mental function Listen S1, S2, extra heart sounds Feel Warmth, pulse character, precordial movement 15 For purposes of clarity, we are considering airway and breathing issues separately. Examination of pulses and circulatory status should occur simultaneously, and will help you better understand the entire clinical picture. When there is time to consider a complete diagnosis or chain of events, this should be done. Below, is a systematic framework for evaluating causes of hypercarbia and hypoxemia. The format is consistent with others used throughout the text: Physiologic roots and their derivations are printed in black; data obtained from labs, data from examination and clinical monitors are noted in red, and likely diagnoses or diagnostic categories are printed in blue. The charts are useful for thinking of problems physiologically, making diagnoses, and prioritizing diagnostics that may differentiate different etiologic categories. Hypoxemia Hypoxemia can manifest itself in a subtle manner, with secondary signs such as change in mentation, delirium, and organ dysfucntion. In such cases the challenge is to correct the hypoxia and figure out why the patient has this problem. Alternately, hypoxia can be intertwined with a primary complaint such as chest pain in major pulmonary embolus, or cardiogenic shock. In either case, your job is to provide rapid stabilization, and address the underlying process as soon as possible. Etiologic categories are listed on the following chart. As with other charts in this text, broad physiologic categories are noted in black, clinical, laboratory and monitor findings are noted in red, and possible diagnoses are written in blue type. 16 Hypoxemia 1. Decreased inspired/ alveolar oxygen Inadequate FiO2 Machine/ tank / pipeline malfunction Altitude Extreme hypercapnea Altered mental status, Agitation Oxygen desaturation CV instability 2. Shunt, increased venous admixture Intracardiac Intrapulmonary Anatomic --liver disease Airway (mainstem intubation) Alveolar (lung injury, hemorrhage, PNA, capillary leak 2o allergy, PE, CHF) 2 3. High Oxygen extraction exacerbated by shunt physiology Decreased SvO2 Decreased CO (see shock fig.) Hemorrhage High VO2 from sepsis, fever, etc 4. Inadequate ventilation Increased CO2 Depressed ventilatory drive Inadequate tidal volume Obstructed airway Tongue, soft tissue (angioedema, OSA, allergy) Airway mass (pharyngeal abscess, epiglottitis, tumor) Laryngeal (tumor, VC paralyisis 2o to nerve injury or hypocalcemia) Machine related (valve, power, oxygen supply) Decrease in compliance of pulmonary system Decrease in Static compliance (Increased P plateau) lung injury, fibrosis, PNA, PTX, pulmonary edema (CHF, large PE) Decrease in Dynamic compliance (Increased P peak) Bronchospasm, mucus plug in airway or in tube, foreign body, hyperinflation 17 Production and Elimination of Carbon Dioxide Carbon dioxide content is one of the primary determinants of acid / base status. Obtaining an ABG is essential to understanding CO2 levels, as well as assessing their contribution to body pH. Abnormally high or low paCO2 values, and deviations from baseline values can often provide a valuable window into the patient’s ventilatory status. Total ventilation (denoted by convention as V E) consists of ventilation of alveoil (VA) as well as non-perfused parts of the lung (dead space ventilation, VD), such that VE = VD + VA. Many critically ill patients have exhaled CO2 sampled and displayed on the bedside monitor; the value displayed (usually referred to as the end tidal CO2). is a useful adjunct to arterial CO2 monitoring. The ET CO2 is always going to be less than alveolar CO2 by a “gradient” that is 5-7 mm Hg in normal subjects, but increases in proportion to increases in VD/ VE. Patients with emphysema, for example, may have a gradient of 15. Patients with a shallow respiratory pattern will also have a higher gradient. Hypocapnea Low CO2 tensions acutely causes a decrease in cerebral blood flow, with attendant changes in mental status or consciousness. Alkalemia if present, can cause coronary vasospasm, bronchoconstriction and a left shift in the oxyhemoglobin dissociation curve. Causes of hypocapnea that you will commonly see are pain, anxiety, and as compensation for metabolic acidosis. Hypercapnea Hypercarbia often manifests as a depressed mental status, tachypnea, hypertension, tachcardia, and ectopy. Increases in CO2 are attributable to either decreased elimination of CO2, increased production, or both. The various etiologies and clinical findings that fall into these general categories are described below. Increased Production of CO2 (usually increased VE –usually normal to increased paCO2) Non-febrile Hyperalimentation, Inadequate anesthesia or sedation, Excessive shivering Febrile Fever, sepsis with poor CO2 elimination Thyrotoxicosis Malignant Hyperthermia (MH), neuroleptic malignant syndrome (NMS) 18 Decreased Elimination of CO2 (increase in dead space) I. Unable to eliminate CO2 from lungs: ( increased VD/VE, decreased VA/VE, RR usually rapid) Inadequate tidal volume Respiratory muscle fatigue Obstructed airway (mechanical, inflamatory) Residual paralytic effect Hypothermia Myxedema coma II. Unable to get CO2 to the lungs (Tidal volume usually normal [ > 8mL/ kg ideal body mass], RR usually rapid; end tidal CO2 variable, depending on the chronicity of the problem) a. Regional Pulmonary blood flow Pulmonary embolus ARDS Emphesema, blebbing b. Generalized Decrease Cardiac Output MI PTX PE Exsanguination 19 Therapy for Respiratory Problems Therapy for Airway problems I. Foreign body Scoop and sweep, forceps removal Heimlich maneuver II. Soft tissue or tongue obstruction, over sedation Chin lift, jaw thrust Supplemental high flow oxygen (100% non-rebreather bag @ 15 L/ min) Nasal and / or oral airway Reverse paralytics and sedatives Benzos--Flumazenil, 0.2 mg IV push, repeat up to 1.0 mg Non-succinylcholine paralytics--5mg neostigmine + 1.0 mg glycopyrolate Opiates--40-80 mcg naloxone, repeat as needed (note: a typical vial contains 400 mcg) Bag-assist ventilation via Ambu Bag or Jackson-Reese circuit (need to call anesthesiologist for help) III. Stridor, (extrathoracic airway obstruction edema,tumor, infection, VC paralysis) Supplemental high flow oxygen (100% non-rebreather bag @ 15 L/ min) Immediate call to anesthesiologist; s/he will help you determine need for surgical airway Need to avoid stimulation and stress; this increases turbulence of airflow Bag-assist ventilation via a Jackson-Reese circuit or BiPAP machine (need to call anesthesiologist for help, AMBU bag may not work without addition of a PEEP valve) Call for expert help with airway management: anesthesiology and ENT Call RT for Racemic EPI, possible heliox (B2- agonists are not appropriate for upper airway obstruction) ABG Therapy for Breathing problems I. Apnea, drive problems Bag-assist ventilation via Ambu Bag and O2, use airways as needed Consider presence of paralytics and sedatives, reverse Benzos--Flumazenil, 0.2 mg IV push, repeat up to 1.0 mg Non-succinylcholine paralytics--5mg neostigmine + 1.0 mg glycopyrolate Opiates--40-80 mcg naloxone, repeat repeat as needed (note: a typical vial contains 400 mcg) ART line if repeat ABGs are likely 20 Intubate if condition not readily reversible Consider brainstem infarct or stroke, herniation: CT scan II. Airflow problems Assess severity, assess CO2 changes in response to inspired O2 Unilateral, consider tumor or foreign body, obtain CXR Diffuse, use bronchodilators, supplemental O2, steroids, IV Epi 10ng/kg/min ART line if repeat ABGs are likely May need to intubate or use BiPAP if work of breathing exceeds strength and reserve III. Excessive work of breathing (Rapid-shallow pattern) BiPAP or mechanical ventilation ABG Exam directed to rule out PTX CXR Consider ART line if repeat ABGs are likely Evaluate for metabolic causes of increased respiratory rate • Remember: patients in extremis have a high catecholamine tone (assume an invisible Epi drip at 50-75 ng/kg/min). Any type of sedative, anxiolytic, or induction agent will decrease the catechol drive and cause a rapid circulatory collapse. Placement of an ART line, and assembly of vasoactive drugs and fluids should be done whenever possible prior to intubation. 21 Physiology and Disruption of Oxygen Transport Understanding the physiology of ventilation and oxygen transport is fundamental to the evaluation and stabilization of any critically ill patient. The principles of oxygen transport are also used to sort out diagnostic dilemmas, as a guide to empiric therapy, and to help define end points of therapy. Oxygen delivery (DO2) is the product of cardiac output and arterial oxygen content (CaO2) as described in the equation below (see box), and under normal conditions greatly exceeds the demand for oxygen (VO2, per minute oxygen uptake or utilization). Under normal conditions we function with a great deal of physiologic reserve where the oxygen supply–demand relationship is described by the right portion of the curve below. As oxygen delivery decreases in the supply-independent region, and while oxygen consumption (VO2) remains constant, more oxygen is extracted per volume of blood at a given time. In low cardiac output states and in hemorrhage, this is appreciated by a decrease in mixed venous O2 saturation from the normal value of 70 percent. When oxygen delivery decreases into the supply-dependent region, mitochondrial respiration is limited by oxygen delivery, and a transition to anaerobic metabolism takes place. The value of DO2 which divides the supply-dependent and supply-independent regions is termed the critical oxygen delivery threshold. 22 Blood pressure is maintained within a certain range for each individual by homeostatic mechanisms that include antonomic reflexes, capillary fluid shifts, and modulation of neurohormones. Blood pressure is important to the body because the various solid organs have adapted their ability to maintain constant blood flow to a certain range of blood pressures (autoregulation, see figure below). For healthy, normotensive people the brain and kidney autoregulate their blood flow at mean pressures between 50-150 mm Hg (black curve in the figure below). However, many of our patients have curves shifted to the right-meaning that kidneys, brain and brainstem, etc., may need higher pressures in order to maintain uniform tissue oxygen delivery (the curve on the right). The overall autoregulatory range of your patient needs to be deliberately considered, and can be inferred in many cases, by a combination of bedside examination and inspection of historical blood pressure data and its correlation with organ function. Poorly controlled hypertensives have fairly dramatic right shifts to their autoregulatiory curves. Shock results from a mismatch between oxygen supply and demand, the latter leads to changes in cellular function that may be either short-lived or permanent. A normal BP does not assure normal oxygen delivery, and vise versa. For example, when hemorrhage exceeds 20% of blood volume, will one likely see a decline in BP. Likewise, the high cardiac output seen in many septic patients often contributes to an adequate oxygen delivery, but at a blood pressure that is beneath the renal autoregulatory set point. Both scenarios can lead to organ failure. 23 Conditions that require evaluation of oxygen delivery status: Bedside findings Hypotension Oliguria Tachycardia Tachypnea Fever Hypothermia Lethargy Confusion Abnormal laboratory findings Elevated anion gap Anemia Acidemia Lactic acid elevation Increase in Creatinine or liver enzymes Decreases in oxygen supply cause a short term transition to anaerobic metabolism; glycolysis without oxidative phosphorylation is unable to sustain ATP production and cell health for prolonged periods. When cardiac output or blood pressure is too low for prolonged periods or when cytokine levels are elevated, endothelial damage occurs, and microvascular thrombosis further impairs capillary blood flow. The pathophysiology of single organ failure by either sepsis or hypoxic damage involves the unleashing of biochemical mediators and other processes (cytokine release, neutrophil and mononuclear cell activation, endothelial cell dysfunction and microvascular thrombosis) that can lead to organ failure at distant sites. For example, hemorrhage or abdominal sepsis can lead to ARDS. Overall, organ failure is further accelerated by prior injury or vulnerability— for example, renal failure or atherosclerotic disease of any major vascular bed. Known solid organ vulnerability should push one toward early aggressive therapy. 24 Circulatory Shock: Strategies for Evaluation and Stabilization Change in mental function, agitation, oliguria, chest pain, and tachypnea are common clinical findings that are usually seen in the natural history of shock and organ failure. When called to evaluate patients with such complaints, the tendency is to hang on to some reassuring sign (such as normal mental status) and then assume all is well and not seek any additional information. A preferable approach is one that assumes something is wrong until proven otherwise. Since the patient is at highest risk for cardiopulmonary arrest if there are problems with oxygen assimilation and transport, understanding the status of these processes should quickly follow the initial ABC survey. Much of what follows is further elaboration on the general ABC-VDE scheme presented earlier in Immediate Assessment and Stabilization. A point to always remember is that problems with oxygen delivery leading to organ dysfunction are not always accompanied by hypotension. Indeed, this point is consistent with current recommendations that lactate levels be measured in septic patients and if abnormal, used as a trigger for early aggressive therapy. 19 Lactate is essentially, an convenient measure of the VO2 / DO2 relationship that can be further corroborated with measurement of mixed venous oxygen saturation. Patient Care Priorities Stabilize airway and breathing, administer appropriate oxygen Look for circulatory abnormality—cardiovert if needed; call for help Obtain vitals and oxygen saturation Obtain appropriate IV access Address tissue oxygen delivery with ABG Consider other studies: stat glucose if pt. is unresponsive, ECG, electrolytes Use physical exam to evaluate CO, SVR, blood loss, pulmonary function AB C V D E BC Treatment for stroke, myocardial infarction, hemorrhagic trauma and major pulmonary embolus are surrounded by the concept of a “golden hour” or similar time frame within which treatment should be instituted. Treatment of hypotension, organ dysfunction, sepsis, and most other medical conditions lack clear time guidelines. Even with this being the case, it’s hard to think of any physiologic abnormality for which it is acceptable to leave the bedside before being corrected. Decisions regarding whether a patient belongs in an ICU or step down unit, the rapidity of resuscitation, how to budget your time, and whether to call in help depend not only on the current vital status, but also on the extent of organ dysfunction. A general inventory of end-organ function can be gained by considering the question on the chart below. 25 Evaluation of Tissue Function and Oxygen Delivery Question Is oxygenation and ventilation normal? Is the body in an anaerobic mode? Is the problem with bound oxygen? Is cardiac output adequate How Addressed O2 sat, PaO2, PaCO2 pH, base deficit, lactate, anion gap Hemoglobin, co-oximetery SvO2 or surrogate, capillary refill, pH in presence of normal [Hb], cold patient Most blood gas analyzers can answer all of these questions with a single sample Other supporting data can come from exam and laboratory findings that address “organs at risk:” CNS or brainstem injury? Metabolic abnormalities? Renal function? Liver function? Orientation, memory, respiratory pattern Electrolyte analysis, anion gap, lactate Creatinine and urine output Tansaminases, bilirubin, PT, PTT Treating hypotension or a low perfusion state is usually accomplished with a combination of fluids, blood, inotropes, and direct vasopressors. The most appropriate choice in a given situation hinges on whether the problem is one of preload, anemia, contractility, or lack of vascular tone. After quickly establishing the presence of a blood pressure or organ blood flow problem, it becomes essential to understand its root cause. The figure on the following page breaks down decreases in BP and DO2 into their constituent parts. As with similar figures in this text, physiologic roots are printed in black, findings from monitors, labs and exam are in red, and common diagnoses for each category are printed in blue. While some of the physiologic data is presented as values obtainable by way of a pulmonary artery (Swan-Ganz) catheter, having such a catheter is not considered a necessity in caring for the critically ill. What is important is to ask the right physiologic questions and to assemble them in a coherent picture. Life Without a Pulmonary Artery Catheter: Examining Physiology by Physical Exam CO Cold extremities, distant pulses, acidosis, SvO2. Try to figure out whether a decrease in CO is due to hypovolemia or due to pump failure. Pump Failure Distended neck veins, S3, cold extremities Preload (CVP) Flat or absent neck veins, tachycarida. Preload (CVP) jugular vein distention, enlarged veins elsewhere SVR BP and mental state may be NORMAL. Findings: Cold extremities, distant pulses. Often a compensation for low preload and/ or low CO. SVR Hypotension is likely. Patient may be warm with full pulses if CO is normal or elevated. Other valuable studies: Spot Echo exam of the heart: addresses tamponade, CHF, ischemia, hypovolemia O2 saturation from CVP line or PICC line: provides indirect but meaningful estimates of the adequacy of DO2, cardiac function. 26 Shock / Hypotension Diagnostic Tree Oxygen delivery (DO2) Lactic acidosis pH, anion gap, BE Peripheral cyanosis end organ function Blood Pressure or or SVR Sepsis Spinal shock Anaphylaxis Heatstroke Iatrogenic Cardiac Output or Heart Rate Arterial Oxygen Content-Hemorrhage, Anemia Severe hypoxemia Stroke Volume Decreased effective stroke volume--classes of abnormalities 1. Contractility: MI, Cardio shock, ( CVP, PaOP, SVR) 2. Preload / filling PTX, tamponade, ( CVP, var PaOP, SVR) Hypovolemia, hemorrhage ( CVP, PaOP, SVR) Tachycardia, dysrhythmia (loss of “atrial kick”) 3. Obstructive: Pulm Embolus, ( CVP, SVR) High PVR with RV failure, ( CVP, PAP, SVR) High SVR, or AS with LV failure ( CVP, PaOP, SVR) Goals : Stabilize BP with empiric fluids and vasopressors Identify etiology and treat more specifically Exception: Arterial ruptures: AAA, dissection, intracranial bleed 27 Therapy for Hemodynamic Instability Unstable patients require simultaneous diagnosis and treatment of underlying physiologic derangements. In evaluating an unstable patient, it becomes crucial to develop some sense of how soon you need to normalize a patient’s status (5 minutes, 10 minutes, one hour?). This type of decision can be made quickly, based on known medical problems, what is know about the acute condition and its natural history, and the patient’s current status (acidotic, ST changes, chest pain, oliguria, hypotensive, etc.). For example, you may be able to show a bit more patience in waiting for fluid infusion to normalize the blood pressure in a young patient with an infection, than in an elderly patient who also has renal insufficiency, cerebral vascular disease, or coronary disease. If in doubt, treat early. Resuscitation and supportive care of many critically ill patients ends up using a careful combination of fluids, inotropes, and vasopressors, based on considerations of the patient’s cardiac status, normal blood pressure, and current status of oxidative metabolism and solid organ function. The typical manner for maximizing cardiac performance, oxygen delivery and blood pressure is in order: titrate in fluids, evaluate cardiac output and use inotropes as indicated, and finally use alpha agonists to maintain blood pressure in an acceptable range. Because you’re not going to arrive at this “solution” immediately, you are certainly justified in treating an abnormally low blood pressure by making crude estimates of filling pressures, cardiac performance, and SVR and giving fluids or vasoactive drugs according to your hunches. This will keep your patient alive in the short term, and buy you some time to get it right later. In attempting to maximize oxygen delivery, often one forgets the need to minimize oxygen consumption. The table below gives some examples of how certain stresses can increase oxygen demand. Condition % Increase Over Resting VO2 Fever 8% (for each 1C increase) Incr. Work of breathing (COPD) 40% Severe Infection 60% Shivering 50% - 100% Burns up to 100% Endotracheal tube suctioning 27% Sepsis 50% -100% Head injury, patient sedated 89% Head injury, patient unsedated 138% Thus, seemingly insignificant acts such as keeping the patient warm, treating fever, and planning diagnostic procedures can be as efficacious as increasing cardiac output with fluids or inotropes. A patient with a severe metabolic acidosis 28 or lung injury can have about 30% of his oxygen consumption dedicated to the work of breathing. In other conditions where pulmonary compliance is poor, the amount of work required to maintain a reasonable minute ventilation can be likewise astronomical. When blood flow to vital organs is compromised, institution of mechanical ventilation will “free up” diaphragmatic blood requirements, and increase the oxygen available to the rest of the body. Mechanical ventilation should be seriously considered on these merits alone, independent of lung injury. On the following pages, a more general scheme for early resuscitation of hypotension and shock is presented. 29 Shock / Hypotension Treatment Outline The goal of most resuscitative strategies is rapid normalization of blood pressure and oxygen delivery. The plan for complete resuscitation and normalization of blood pressure is more negotiable in cases hemorrhagic shock, cerebral hemorrhage, and arterial bleeding.16 Rapid identification of such processes and consultation with an appropriate service is a high priority, and discussions regarding resuscitation end points should take place quickly. Likewise, suspicion for cardiogenic shock should lead to immediate consultation with cardiology regarding early revascularization.17 Following the ABC-VDE evaluation, use the guide below as a checklist and a guide to pharmacotherapy. Different centers may have different methods and protocols for resuscitation. Whichever you end up using, the most important thing is that you make a constant cycle between: a plan for action the action an assessment of the action and its impact and a reassessment of the situation which leads to the next plan of action, and so on. In the business world, this is known as a PDSA cycle for “plan, do, study, act.” Priority #1. Normalize Blood Pressure: Crystalloid fluid: 1-2L over 10-15 minutes. 2 X 18g, or 16g or percutaneous introducer. May need pressure bag. Triple lumens are generally inadequate. Vasopressor or inotrope to maintain oxygen delivery and BP. Want to normalize BP in 2-5 minutes after IV access is established. A new stable peripheral IV or PICC line is OK to use for initiial use of vasopressors. • Phenylephrine 100mcg IV q 1-5 minutes (may HR) • Ephedrine 5-10mg q 3-5 minutes (will HR) • Epinephrine 10-30mgc IV q 2-5 minutes (will HR) • Dopamine 3-10 mcg/kg/min. May need bolus of phenylephrine or ephedrine until target dopamine levels are achieved Place Art line. Consider femoral (16g single lumen) if MAP < 55 Place central line for CVP, vasoactive drips, venous 02 saturation Priority #2. Define nature and severity of injury: Labs and Diagnostics: Exam: ABG skin color and warmth CBC, PT/PTT*, DIC*, pulse character Lactate alertness, memory Electrolytes including glucose breath sounds Mixed venous O2 heart sounds Type and screen* pain CXR* subjective complaints EKG,* Echo* evidence of bleeding Cultures* *as indicated by clinical situation Priority #3. Treat underlying cause as soon as it is known or suspected: Antibiotics, Gluccocorticoids, Blood and fluid replacement See reference 18 for further review of evidence for treatments for septic shock 30 Acute Blood Loss Patients may experience sudden and massive blood loss for a variety of reasons-the most common being traumatic injury and/or surgical blood loss. However medical patients can also experience sudden and massive blood loss (i.e. GI bleed, hemoptysis, leaking AAA) and thus require an expeditious resuscitation to reduce morbidity and mortality. Traumatic blood loss and resuscitation is an especially dynamic process involving factor and fibrionogen consumption, dilutional coagulopathy, and further interaction between the coagulation system, temperature, and anoxic tissues. A full discussion on the management of hemorrhagic shock is beyond the scope of this text; instead, the concentration will be on non-traumatic blood loss. When faced with massive and sudden blood loss in a patient, one should immediately call for help to mobilize all available resources. Help includes fellow residents, a stat surgical consult, anesthesia, crisis/ICU nurses, and the ICU fellow/team. Initial patient assessment should include ABCs assuring an adequate airway and placing the patient on 100% oxygen. Circulation should be assessed with the goal of aggressive treatment of tachycardia and hypotension with IV fluids. Stat laboratory tests for CBC, ABG, coags, lactate, and type/cross should be drawn immediately by bedside personnel and taken directly to the lab for urgent processing. Care team members should establish adequate IV access,14-16g peripheral IVs or a “Cordis” introducer for rapid fluid administration. A triple lumen cath is inadequate. If present and it is difficult to find additional access consider changing to an introducer over a wire. Nurses should be alerted that you want blood pumps connected to blood warmers so that these will be ready at the time you place the IV lines. If blood is needed immediately, before the blood bank has time to set up type and crossed units, send a runner to the blood bank and request a “trauma bucket” which should contain 6 units of O negative blood. Ideally type and crossed blood should be given. In the event that is not ready, then type specific uncross-matched blood is preferable followed by O negative. As the initial resuscitation proceeds, plans for definitive treatment of the bleeding should be made (i.e. OR/cath lab, etc) as well as transfer to the ICU for further care and management. Depending on the rate and amount of the blood loss you may have to replace the circulating blood volume several times until the bleeding is controlled. As one approaches 1.5 blood volumes transfused (adult range of 7-8 liters), a dilutional thrombocytopenia and coagulopathy may develop. Expect to give fresh frozen plasma (FFP) and platelets after two blood volumes have been transfused or earlier if there is laboratory evidence to suggest a more aggressive transfusion need (platelet count less than 80 or PT/PTT greater than 1.5x normal). FFP, if given in adequate volume, should replace clotting factors and fibrinogen. However, if the fibrinogen continues to be less than 1.0 g/L then 31 cryoprecipitate should be considered. Throughout the resuscitation heart rate, blood pressure, SaO2, mental status, and urine output should be monitored continuously (consider Art line/CVP). Throughout the resuscitation, heart rate, blood pressure, SaO 2, mental status, and urine output should be monitored continuously (consider Art-line / CVP / foley). Rapid Transfusion Rapid transfusion of large volumes of stored red blood cells can result in several potential dangerous complications. When the rate of transfusion exceeds 1 unit every 5 minutes there is a risk of hypocalcaemia from citrate toxicity. Signs of hypocalcaemia include hypotension, flat T waves, prolonged QT interval and a widened QRS complex. This should be treated with 500-1000 mg of IV CaCl2 via a central line or calcium gluconate via a peripheral IV. The reduced concentration of 2,3-DPG in the hemoglobin of stored PRBC results in a left shift in the Hb-oxygen dissociation curve and less availability of oxygen at the tissue level. Hyperkalemia can result from increased potassium from lysed red cells in the stored blood. In blood stored greater than 21 days K can be as high as 35 mEq/L. Micro aggregate formation occurs in the stored units and can cause pulmonary insufficiency and ARDS when patients receive massive transfusions (>10 units/24hrs). PRBC are stored at temperatures between 1-6 degree C. Failure to use a blood warming device can result in significant hypothermia. This can result in increased risk for the development of DIC, and less activity of existing clotting factors. Furthermore, hypothermia is associated with a higher mortality rate in massively transfused patients. Failure to warm the blood prior to transfusion can result in significant hypothermia. Replacement of red blood cells should take priority over coagulation factors when resuscitating the acutely hemorrhaging patient. Acute pain 32 There is no diagnostic or therapeutic yield in leaving a patient in pain. Major abdominal pathology, dyspnea and bone pain can still undergo appropriate evaluation without the added distress of nociception. Some points on the practical physiology of pain can be summarized: The perception of pain is highly subjective and cannot be easily quantified across a heterogeneous population. Pain is a significant stimulant of the sympathetic nervous system, and can exacerbate coronary and vascular pathology. Pain exacerbates psychiatric pathology. Controlling pain later is generally more difficult than treating at the earliest opportunity. Poorly controlled pain can lead to other limb-pain syndromes or chronic pain. Agents such as NSAIDS and acetaminophen are terrible PRN drugs, but great as round-theclock agents in a comprehensive pain control scheme. Opiate tolerance is not opiate addiction, and may be acceptable in the short term. Like other abnormalities in the vital status, extreme pain needs to be controlled acutely at the bedside. Here is an example of the acute management of incisional pain: Fentanyl in 25-50 mcg boluses are given to the opiate naïve person with a small incision; 50-100 mcg with a younger patient, 100-200 if opiate tolerant. Look at prior dosing histories to get some idea of tolerance and effective doses (cath lab reports, anesthesia records and ER sheets). Continue boluses every 2-4 minutes until the pain score becomes 2-3. Give a few doses of morphine 2-5 mg and monitor for respiratory depression. A nurse can continue with morphine 2-5 mg q 15 min, until a PCA is ready. Drug _______ Morphine Fentanyl Dilaudid Meperedine Vicodin Methadone Equianalgesic Dose 10 mg 100mcg 2 mg 75 mg 8 tablets 10 mg Cautions / notes Venodilation via histamine mechanism, n/v, pruritis No venodilation Less pruritis and n/v than morphine Aviod for pain, use 25-50 mg for shivering & rigors 4g Acetaminophen at this dose--don't exceed No role for acute control Some like morphine for acute coronary syndromes because its venodilatory property also lowers myocardial wall stress. Reversing opiates The ER uses 0.4 mg of Naloxone to reverse possible opiate effects in comatose patients. For the respiring patient, this is too high a starting dose. Overdosing naloxone will make your patient absolutely wild, and produce a dangerous hypertensive crisis. 1/10 of a vial (40 mcg) in q 1-2 minute escalating doses will reverse respiratory depression without antagonizing the analgesic properties. 33 Leadership in Medical Emergencies. The team leader has a difficult role and to make matters worse, medical education offers nearly zero preparation or training for this role. ACLS training gives the impression that if you can make the right diagnosis and apply the correct algorithm with a certain amount of precision, everything else falls into place. Anyone can walk into a room and say “give epi,” but is that realistic? Who has the epi? Is someone placing an IV? Is there fluid to hook up to the IV when it’s in? Is the same person who is doing all of the above the only one who knows how to give drugs, work the monitors, and hook up pacing pads? Managing the chaos of a code or resuscitation is always hard to script out, but some key principles of communication and resource allocation are useful to consider and will serve you well: Know your environment. Know your team and their capabilities—don’t assign tasks to non-experts whenever possible. Get better help if you are unsure. Distribute the workload evenly, don’t create “bottlenecks” where only one person is asked to do things or has the knowledge to get things done. Don’t get involved in procedures, CPR, or other tasks that would distract you from your leadership role or your ability to take in the “big picture.” Communicate your general thoughts and priorities to the team. Get help if you need. Establish goals, and allow some autonomy in reaching those goals. For example: • give the nurse a range of doses to work with to reach a goal, state the goal. • allow respiratory therapist to do whatever is takes short of intubation to improve respiratory mechanics or O2 saturation. Focus on significant actions, do not occupy skilled personnel with insignificant tasks. Don’t spout commands into the air. Calmly ask people to do things using their names and eye contact. If more than one task is assigned, establish priorities. Monitor who is doing what; follow up with individuals on progress at appropriate intervals. You can’t learn this overnight—well, maybe you can, but I can’t! Some of the best ways to train for emergency leadership are to (1) observe others who are good at it and spend some time thinking about specific things that seemed unusually good, (2) practice in a controlled environment with proper mentorship (simulation), and (3) to understand all of the different roles and tasks required by a resuscitation. The latter can be achieved by going to codes and performing specific tasks (lines, ABG, chart review), and seeing how these tasks mesh with other parts of the operation. Likewise, just watch what specific people are doing and ask yourself whether they are effective or not, overloaded or under loaded, assigned tasks commensurate with their level of skill, etc. By knowing everything that goes on in an urgent situation and the times and struggles associated with each, you will have 34 a more realistic idea of what you are asking others to do and how much time and attention different tasks take. The other side of leadership is knowing when to step back and look things over. You may arrive at a scene where there is already adequate leadership. Don’t let you job description get in the way of the best patient care. Your job isn’t running the show as much as putting the patient first and doing what’s best for that person’s survival. Use your leadership skills to support the existing efforts if they appear to be on target. As you view a resuscitation effort, think about what gaps in information or care exist, and make yourself useful by filling in these holes. V. Treatment--General approach Treatment decisions depend upon your goals, expectations, and what you think the patient needs or can tolerate. It is important to have a sense of time: how long the patient can last as is, and how fast things need to be corrected. Your choice of agents will be impacted greatly by your time goals. What abnormalities require treatment? Any abnormal vital sign deserves your attention. But despite our ability to rapidly normalize many aspects of our patients’ status, and that generally stabilization should precede an exact diagnosis, the underlying diagnosis will dictate the appropriateness of different treatment options and the overall goal of treatment. Some exceptions to aggressive normalization of vital status are presented below. Anormality Hypotension Tachycardia& Bradycardia Circumstances that may modify treatment plan Arterial rupture; out of hospital trauma. Proceed to surgery before full resuscitation. If CHF, consider baseline BP (is this a result of therapeutic afterload reduction?) Sepsis, hypovolemia, anemia. See notes below& Hyperthermia Consider observation over treatement if rhythm is NSR, patients is hemodynamically stable or hypertensive; w/ aortic stenosis or severe CAD Always treat in some way. Can get late respiratory depression when adding IV opiates to epidural or spinal opiates. NSAIDS and renal; Tylenol and liver dz. Modify treatment with head injury or with increased ICP. Caution; reflex tachycardia with vasodilators. Beta block first with arterial injury or aneurysm. Very hot or very sick may require aggressive treatment Hypothermia May be best untreated with brain injury or CVA if tolerated by heart. d/w neuro Acute pain* Hypertension Hypopnea May be necessary side effect of difficult to control pain; assess deep breathing, airway, and alertness for danger signs; expect some resp. acidosis SaO2 < 95% Consider patient's baseline if COPD present. -------------------* Always perform careful assessment; otherwise normal vital signs do not "rule out" a catastrophic process. & Sinus tachycardia in hospitalized patients is rarely a primary abnormality. It likely reflects a compensatory mechanism. First, find the underlying cause, and treat tachycardia only if it is acutely appropriate. Rate control of rapid A-fib is usually beneficial. 35 Regardless of abnormality, your response as the leader should be the same: Assess Plan Treat Re-assess Plan Treat Re-assess You need to treat a clinically significant vital sign abnormality in a single encounter. If you are at a computer placing an order and not at the bedside with a syringe in hand, you have missed this point. Having an idea of entry-level doses and kinetics is important, as you don't want to overlap doses of agents when the first hasn't had the opportunity to work. Also, be extra careful when your patient has a low cardiac output; the usual heart-to-end organ circulation time can be significantly delayed, creating an impression that the patient didn't respond to the previos dose. Drug Entry-level dose Onset Fentanyl Morphine Morphine PCA Nitroprusside (drip) Nitrglycerin (drip) Phenylephrine Phenylephrine (drip) Dopamine (drip) Epinephrine (drip) Epinephrine (with pulse present) Ephedrine 25-50 mcg 1-4 mg 1-4 mg q 10 min (0.2-0.3 mcg/kg/min) (0.2-0.3 mcg/kg/min) 50-100 mcg 10-25 mcg/ min 2-3 mcg/kg/min 10-50 ng/kg/min 20-50 mcg 5-10 mg 3-5 minutes 10 min 2-3 hrs 3 min 3 min 1-2 min 4-10 min 5-10 min 3-10 min 45 sec-1.5 min 1.5-2 min General template for crisis management and leadership Different clinical situations require specific configurations of the treatment team. A generic list of priorities and potential task distributions is presented as a vehicle to stimulate further thinking on your part. 1. Know your team and environment—who can provide what kinds of help?? Task or knowledge base Drugs, doses and routes: IV and arterial access Respiratory support Chart review Lab data retrieval Vital signs Physical exam Potential help Pharmacist, anesthesiologist (consider phone call in urgent situation) Anesthesiologist, surgeon, ICU nurse, ICU fellow Resp. therapy, RN, anesthesiologist Medical student and above RN, Nurse assistant, medical student or above Nursing student, med student and above Med student or above, preferably Intern 36 Distribute the workload as evenly as possible. Pair the most highly trained personnel to the tasks with the highest pressure or skill requirement. If in doubt, ask your team if they are totally comfortable doing what they were assigned to do. Call your attending for additional support. 2. Assign someone to obtain vital signs at an appropriate interval. Establish data streams and understand their source (Know how frequently the BP cuff is cycling. Know what ECG leads you are observing. Know what lines the patient has and if data is being displayed. Know where the pulse ox is connected to the patient. Know what labs have been drawn, what recent data shows. Assign someone to watch monitors, assign parameters to be reported back to you. 3. Establish relative priority for diagnostic and therapeutic efforts. Consider compartmentalizing diagnostic and therapeutic efforts. Careful to not overload team members. 4. Consider the need for urgent consultation with other services and call others at a time when their efforts can make a difference. Keep in mind that interventional radiology, the cath lab, and the operating room are complex services that require significant “set up time.” Factor these time delays into your therapeutic plans 5. If in doubt, start early aggressive stabilization of: • hypovolemia • hypotension • hypoxemia • hypopnea or tachypnea • MI and cardiogenic shock (tachycardia in inpatients is rarely the primary abnormality, do not treat it unless the BP is normal). 6. Make best estimate of underlying problem (blood loss?, infection?), begin empiric therapy 7. Establish therapeutic goals (how quickly to normalize BP, etc). 8. Pursue diagnostic information as needed to influence plan. 9. Communicate priorities and plans, keep team focused. Make sure your team members are communicating any difficulties they are encountering. Reassign tasks as needed. 37 References: 1: Volpp KGM, Grande D. Residents' suggestions for reducing errors in teaching hospitals. N Engl J Med 2003;348:851-855. 2: Goldhill DR, Sumner A. Outcome of intensive care patients in a group of British intensive care units. Crit Care Med. 1998 Aug;26(8):1337-45. 3: Sax FL, Charlson ME. 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