(BQ) Part 2 book Critical care medicine the essentials has contents: Venous thromboembolism, obstructive disease and ventilatory failure, thermal disorders, hepatic failure, drug overdose and poisoning, neurologic emergencies,... and other contents.
Chapter 20 Cardiopulmonary Arrest • Key Points The success (hospital discharge without neurological impairment) of cardiopulmonary resuscitation is highly variable among patient populations Cardiopulmonary resuscitation is very effective when applied promptly to patients with sudden cardiac death because of electrical instability, but is quite ineffective when applied in chronically debilitated patients and those suffering arrest as part of the natural progression of multiple organ failure The goal of resuscitation is to preserve neurological function by rapidly restoring oxygenation, ventilation, and circulation to patients with arrested circulation The resuscitation status of every patient admitted to the ICU should be considered at admission When a clear determination regarding resuscitation status cannot be made quickly, the physician generally should err on the side of promptly initiating resuscitation efforts Obvious exceptions to this recommendation apply when cardiopulmonary resuscitation is prohibited by patient mandate or not indicated because it cannot produce successful results Most successful resuscitations require only to minutes In these, establishing a patent airway and promptly applying direct current shocks to reestablish a perfusing rhythm are the key actions necessary It is quite uncommon to successfully resuscitate a patient after more than 20 to 30 minutes of effort A notable exception to this rule occurs in patients with hypothermia who are occasionally resuscitated after hours of effort Although widely published guidelines provide a framework for resuscitation, cardiopulmonary arrest in a hospitalized patient often has a specific cause; therefore, resuscitative efforts should be individualized Common situations are outlined in Table 20-1 In most cases, reestablishing an effective rhythm involves either the application of direct current shocks to terminate ventricular fibrillation or tachyarrhythmia or the acceleration of bradyarrhythmias Although the systemic acidosis seen in patients with circulatory arrest can be buffered with NaHCO3, a better strategy is to optimize ventilation and circulation NaHCO3 should not be used routinely but retains a role for specific arrest circumstances such as tricyclic antidepressant overdose, hyperkalemia, and extreme acidosis By necessity, most recommendations for treating cardiopulmonary arrest are not derived from highquality randomized human studies but rather from retrospective series, animal experiments, and expert opinion Treatment recommendations traditionally have been most applicable to patients who sustained sudden cardiac catastrophes, especially those occurring outside the hospital Because the focus of this book is on the hospitalized critically ill patient, some of the discussion that follows will naturally differ from widely disseminated recommendations Most arrests among patients with ischemic heart disease are due to ventricular tachycardia (VT) and ventricular fibrillation (VF) As a corollary, because pulseless VT or VF is so likely to be the cause of death in the cardiac ICU, such patients should almost always be treated immediately with unsynchronized cardioversion By contrast, a respiratory event (aspiration, excessive sedation, pulmonary embolism, P.422 P.423 airway obstruction) is much more likely to occur at other sites in the hospital It follows that arrests on a hospital ward or noncardiac ICU are more likely to respond to a directed intervention beyond a cardiac rhythm change, often one involving the lungs Table 20-1 Common Clinical Scenarios of Cardiopulmonary Arrest Setting Likely Etiology Appropriate Intervention During mechanical ventilation Misplaced ET tube Tension pneumothorax Hypovolemia Auto-PEEP Hypoxemia Mucus plugging Confirm proper location by visualization and auscultation, CO2 detector Physical examination, chest tube placement Fluid bolus Reduce minute ventilation, increase expiratory time, bronchodilator, suction airway Check ET tube placement, oximeter saturation; administer 100% O2 Suction airway Postcentral line placement/attempt Tension pneumothorax Tachyarrhythmia Bradycardia/heart block Physical examination, chest tube placement Withdraw intracardiac wires or catheters; consider cardioversion/antiarrhythmic Withdraw intracardiac wires or catheters, consider chronotropic drugs, temporary pacing During dialysis or plasmapheresis Hypovolemia Transfusion reaction IgA deficiency: allergic reaction Hyperkalemia Fluid therapy Stop transfusion; treat anaphylaxis Stop transfusion; treat anaphylaxis During transport Displaced ET tube Interruption of vasoactive drugs Early identification using end-tidal CO2 Restart IV access Acute head injury Increased intracranial pressure (especially with bradycardia) Diabetes insipidus: hypovolemia (especially with tachycardia) Lower intracranial pressure (ICP): hyperventilation, mannitol, 3% NaCl Administer fluid Check K+; treat empirically if ECG suggests hyperkalemia After starting a new medicine Anaphylaxis (antibiotics) Angioedema (ACE inhibitors) Hypotension/volume depletion (ACE inhibitors) Methemoglobinemia Stop drug; administer fluid, epinephrine, corticosteroids Volume expansion Methylene blue Toxin/drug overdose cyclic antidepressants β- Seizures/tachyarrhythmias Severe bradycardia Severe bradycardia Sodium bicarbonate Chronotropes, pacing, glucagon, insulin + glucose Decontamination, atropine, pralidoxime After myocardial infarction Tachyarrhythmia/VF Torsades de pointes Tamponade, cardiac rupture Bradycardia, AV block DC countershock, lidocaine Cardioversion, Mg, pacing, isoproterenol, stop potential drug causes Pericardiocentesis, fluid, surgical repair Chronotropic drugs, temporary pacing After trauma Exsanguination Tension pneumothorax Tamponade Abdominal compartment syndrome Fluid/blood administration, consider laparotomy-thoracotomy Physical examination, chest tube placement Pericardiocentesis/thoracotomy Measure bladder pressure; decompress abdomen Burns Airway obstruction Hypovolemia Carbon monoxide Cyanide Intubate Fluid administration 100% O2 Hydroxocobalamin blocker/Ca2+ blocker Organophosphates Carbamates ABG, arterial blood gases; ACE, angiotensin-converting enzyme; AV, atrioventricular; DC, direct current; ECG, electrocardiogram; ET, endotracheal; PEEP, positive end-expiratory pressure; VF, ventricular fibrillation PRIMARY PULMONARY EVENTS (RESPIRATORY ARREST AND SECONDARY CARDIAC ARREST) Patients found unresponsive without respirations but with an effective pulse have suffered a respiratory arrest Failure to rapidly restore ventilation results in hypoxemia and progressive acidosis that culminates in reduced contractility, hypotension, and eventual circulatory collapse Although the etiology of many respiratory arrests remains uncertain even after thorough investigation, the cause often can be traced to respiratory center depression (e.g., sedation, coma, stroke, high intracranial pressure) or to failure of the respiratory muscle pump (e.g., excessive workload, impaired mechanical efficiency, small or large airway obstruction, or muscle weakness) Tachypnea usually is the first response to stress, but as the burden becomes overwhelming, the respiratory rhythm disorganizes, slows, and eventually ceases Initially, mild hypoxemia enhances the peripheral chemical drive to breathe and stimulates heart rate Profound hypoxemia, however, depresses neural function and produces bradycardia refractory to autonomic influence At this point, cardiovascular function usually is severely disordered, both because cardiac and vascular smooth muscle function poorly under conditions of hypoxia and acidosis and because cardiac output falls as heart rate declines The observation that nearly one half of hospitalized cardiopulmonary arrest victims exhibit an initial bradycardic rhythm underscores the role of respiratory causes of circulatory arrest FIGURE 20-1 Change in arterial partial pressure of oxygen and carbon dioxide after respiratory arrest (normal lungs) Oxygen concentration falls precipitously to dangerously low levels within minutes By contrast, the rise in carbon dioxide tension is much slower, requiring 15 to 20 minutes to reach levels sufficient to produce life-threatening acidosis In many critically ill patients, the arterial partial pressure of oxygen (PaO2) plummets shortly after ventilation ceases because limited O2 stores are rapidly consumed Reserves are diminished by diseases that reduce baseline saturation (e.g., chronic obstructive pulmonary disease [COPD], pulmonary embolism), lower functional residual capacity (e.g., morbid obesity, pregnancy), or both (e.g., pneumonia, pulmonary fibrosis, congestive heart failure) Ambulatory patients who suffer sudden cardiac arrest usually draw upon substantially greater O2 reserves because they typically not have diseases causing significant desaturation or thoracic restriction at baseline For this reason, attention to oxygenation is much more important in the hospitalized respiratory arrest victim, whereas establishing artificial circulation and prompt rhythm correction are priorities for the “cardiac” death patient Unlike O2, CO2 has a huge storage pool and an efficient buffering system Therefore, PaCO2 initially builds rather slowly, at a rate of to mm Hg in the first apneic minute and to mm Hg/min thereafter (Fig 20-1) However, as the apneic patient develops metabolic acidosis from tissue hypoxia, H+ combines with to dramatically increase the rate of CO2 production The net effect of these events is that life-threatening hypoxemia occurs long before respiratory acidosis itself presents a major problem P.424 PRIMARY CARDIOVASCULAR EVENTS (CARDIOPULMONARY ARREST) The heart may abruptly fail to produce an effective output because of arrhythmia or suddenly impaired pump function resulting from diminished preload, excessive afterload, or decreased contractility The normal heart compensates for changes in heart rate over a wide range through the Starling mechanism Thus, cardiac output usually is maintained by compensatory chamber dilation and increased stroke volume despite significant slowing of rate Children and adults with dilated or noncompliant hearts have less reserve and are highly sensitive to bradycardia Decreases in left ventricular preload sufficient to cause cardiovascular collapse usually are the result of venodilation, hemorrhage, pericardial tamponade, or tension pneumothorax In contrast to the left ventricle, which is continually adapting to afterload that changes over a wide range, the right ventricle does not readily compensate for increased impedance to ejection Therefore, abrupt increases in right ventricular afterload (e.g., air or thromboembolism) are likely to cause catastrophic cardiovascular collapse Acute dysfunction of cardiac muscle can result from tissue hypoxia, severe sepsis, acidosis, electrolyte disturbance (e.g., hypokalemia), or drug intoxication (e.g., β-blockers) Regardless of the precipitating event, patients with narrowed coronary arteries are particularly susceptible to the adverse effects of a reduced perfusion pressure Neural tissue is disproportionately sensitive to reduced blood flow Circulatory arrest always produces unconsciousness within seconds, and respiratory rhythm ceases rapidly thereafter Thus, ongoing respiratory efforts indicate very recent circulatory collapse or the continuation of some blood flow, even if below the palpable pulse threshold (In a person of normal body habitus, a systolic pressure of approximately 80, 70, or 60 mm Hg must be present for a pulse to be consistently detected at radial, femoral, or carotid sites, respectively.) CARDIOPULMONARY RESUSCITATION Cardiopulmonary resuscitation (CPR) was conceived as a temporary circulatory support procedure for otherwise healthy patients suffering sudden cardiac death In most cases, coronary ischemia or primary arrhythmia is the inciting event Since its inception, however, CPR use has been expanded to nearly all types of patients who suffer an arrest A general approach currently recommended by the American Heart Associated is presented in Figure 20-2 Note that although this approach presents a general overview of intervention for cardiac arrest, specific interventions and situations encountered in the ICU as described in Table 20-1 must be considered The intensivist is frequently consulted for cardiac arrest occurring on the medical/surgical unit or in clinic spaces of the hospital where this initial approach is applicable Currently, less than one half of all patients undergoing CPR will be successfully resuscitated initially, and less than one half of these initial survivors live to hospital discharge Even more discouraging, at least one half of the discharged patients suffer neurological damage severe enough to prohibit independent living Despite the success portrayed on television, a small number of CPR recipients enjoy even a near-normal postarrest life In addition, pharmacoeconomic analyses suggest that in-hospital resuscitation may be the least cost-effective treatment delivered with any regularity The likelihood of successful CPR (discharge without neurological damage) depends on the population to whom the procedure is applied and the time until circulation is restored Brief periods of promptly instituted CPR are highly successful when applied to patients with sudden cardiac death, but when CPR takes place in the setting of progressive multiple organ failure, the likelihood of benefit approaches zero Principles of Resuscitation This chapter emphasizes enduring principles of resuscitation and intentionally omits details that are not based on convincing evidence or are likely to change Current expert recommendations for resuscitation are much simpler than those in the past and stress the importance of effective circulatory support and prompt shock of pulseless VT and VF while de-emphasizing respiratory support Although that advice makes sense for most out of hospital events, in the hospital, the resuscitation team must quickly consider the specific circumstances of each arrest to determine the best course of action (Table 20-1) For example, a mechanically ventilated patient found in VF will not be saved by P.425 P.426 a formulaic approach to arrhythmia treatment if it is not recognized that the cause of the event is a tension pneumothorax or major airway obstruction Because survival declines exponentially with time after arrest (Fig 20-3), most successfully resuscitated patients are revived in less than 10 minutes To this end, first responders should summon help and begin effective chest compression If the cardiac rhythm can be monitored and is pulseless VT or VF, unsynchronized direct current (DC) cardioversion using maximal energy should be delivered as quickly as possible If these initial actions are unsuccessful, more prolonged, “advanced” resuscitation measures may be indicated FIGURE 20-2 General overview of approach to cardiac arrest This strategy may be modified based on presenting considerations as listed in Table 20-1 CPR, cardiopulmonary resuscitation; IO, intraosseous; IV, intravenous; PEA, pulseless electrical activity; PETCO2, end tidal PCO2; PVT, pulseless ventricular tachycardia; ROSC, return of spontaneous circulation; VF, ventricular fibrillation (Numbers guide progress through this algorithm.) FIGURE 20-3 Probability of successful initial resuscitation after cardiopulmonary arrest Exponential declines in survival result in low success rates after to 10 minutes of full arrest conditions The primary activities of resuscitation include (1) team direction, (2) circulatory support, (3) cardioversion/defibrillation, (4) airway management and ventilation, (5) establishing intravenous access, (6) administering drugs, (7) performance of specialized procedures (e.g., pacemaker and chest tube placement), and (8) database access and recording Managing a cardiopulmonary arrest usually requires several persons to directly execute procedures Additional personnel are needed for nonprocedural tasks such as documentation, chart review, and communication with the laboratory or other physicians, but limiting the number of people involved to the minimum required avoids confusion Principle 1: Define the Team Leader A single person must direct the resuscitation team because chaos often surrounds the initial response This person should attempt to determine the cause of the arrest, confirm the appropriateness of resuscitation, establish treatment priorities, and coordinate the steps of ACLS protocol The leader should also monitor the electrocardiogram (ECG), order medications, and direct the actions of the team members but must avoid distraction from the command role by performing other functions Principle 2: Establish Effective Artificial Circulation Blood flow during closed-chest CPR likely occurs by two complementary mechanisms: direct cardiac compression and thoracic pumping First, compressions generate positive intracardiac pressures, simulating cardiac chamber contraction with the unidirectional heart valves helping to ensure forward flow In addition, as the chest is compressed, a positive gradient is established between intrathoracic relative to extrathoracic arterial pressures, propelling flow forward Retrograde venous flow is prevented by jugular venous valves and functional compression of the inferior vena cava at the diaphragmatic hiatus On relaxation of chest compression, falling intrathoracic pressures promote blood return into the right heart chambers and pulmonary arteries, filling these structures for the next compression Automated systems are available to provide CPR as other cares or patient transfer occurs (Fig 20-4) Regardless of mechanism, even ideally performed closed-chest compression provides only one third of the usual output of the beating heart Thus, when CPR is performed for more than 10 to 15 minutes, hypoperfusion predictably results in tissue acidosis If performed improperly, CPR is not only ineffective P.427 but potentially injurious Several points of technique deserve emphasis Maximal flow occurs with a compression rate of 100 to 120 beats/min Current recommendations have increased the ratio of compressions to breaths in an attempt to maximize flow For the same reason, current protocols suggest continuing CPR for several minutes after electrical shock attempts To optimize cardiac output, it is important to adequately compress the chest Ideally, the anterior chest is depressed by at least in in the adult Timing of the stroke is important: shortduration “stabbing” chest compressions simulate the low stroke volume of heart failure, whereas failure to fully release compression simulates pericardial tamponade or excessive levels of positive end-expiratory pressure (PEEP) Openchest cardiac compression may provide double the cardiac output of the closed-chest technique but presents obvious logistical problems and has not been demonstrated to improve survival FIGURE 20-4 Mechanical system for performance of chest compressions in CPR During CPR, it is difficult to determine whether blood flow is adequate, because pulse amplitude, an index of pressure, does not directly parallel flow and organs vary with regard to the flow they receive at a given pressure For example, brain flow relates to differences between mean aortic pressure and right atrial pressure, assuming normal intracranial pressure Therefore, increasing right atrial pressure will decrease brain blood flow when mean arterial pressure is held constant Coronary blood flow, on the other hand, is best reflected by the diastolic aortic to right atrial pressure gradient For both, vasoconstrictive drugs (i.e., epinephrine) are recommended to raise the mean aortic pressure Principle 3: Establish Effective Oxygenation and Ventilation Establishing a secure airway and provision of supplemental oxygen are essential if the primary problem was respiratory in origin, or whenever resuscitative efforts continue for more than a few minutes Except in unusual circumstances, ventilation can be quickly accomplished in the nonintubated patient with mouth-to-airway or bagmask ventilation Because position, body habitus, and limitations of available equipment often compromise either upper airway patency or the seal between the mask and face, effective use of bag-mask ventilation often requires two people When the airway is patent, the chest should rise smoothly with each inflation Gastric distension and vomiting may occur if inflation pressures are excessive Inflation pressures generated by bagmask ventilation are sufficient to cause barotrauma and impede venous return; to minimize these risks, breaths should be delivered slowly, avoiding excessive inflation pressures and allowing complete lung deflation between breaths In cardiopulmonary arrest, the most common cause of airway compromise is obstruction of the upper airway by the tongue and other soft tissues Thus, in most cases after effective chest compression and ventilation have been achieved, an experienced person should intubate the airway (see Chapter 6) As a rule, intubation attempts should not interrupt ventilation or chest compression for longer than 30 seconds Therefore, all materials, including laryngoscope, endotracheal (ET) tube, and suction equipment, should be assembled and tested before any attempt at intubation Inability to establish effective oral or bag-mask ventilation signals airway obstruction and should prompt an immediate intubation attempt When neither intubation nor effective bag-mask ventilation can be accomplished because of abnormalities of the upper airway or restricted cervical motion, temporizing measures should be undertaken while preparations are made to create a surgical airway The laryngeal mask airway (LMA) is an easily inserted, highly effective temporizing device It is important to have an LMA, which is appropriately sized for the patient If the LMA is too large, it may obstruct the larynx or cause trauma to laryngeal structures An LMA that is too small or inserted improperly may push the base of the tongue posteriorly and obstruct the airway The LMA should only be used in an unresponsive patient with no cough or gag reflex If the patient has a cough or gag reflex, the LMA may stimulate vomiting and/or laryngospasm In unusually difficult circumstances, insufflation of oxygen (1 to L/min) via a large-bore (14- to 16-gauge) needle puncture of the cricothyroid membrane can temporarily maintain oxygenation Phasic delivery of higher flows of oxygen by the transtracheal route also can promote CO2 clearance, but CO2 removal is of much lower priority In the arrest setting, direct visualization of the tube entering the trachea, symmetric chest expansion, and auscultation of airflow distributed equally across the chest (without epigastric sounds) are the most reliable clinical indicators of successful intubation Colorimetric CO2 detectors attached to the ET tube may support impressions of proper tracheal P.428 tube placement; however, because circulation and CO2 delivery to the lungs are both severely compromised during CPR, detectors may fail to change color on many properly placed tubes For the same reason, attempts to eliminate CO2 by ventilation are relatively ineffective During CPR, ventilation should attempt to restore arterial pH to near-normal levels and provide adequate oxygenation Unfortunately, the adequacy of ventilation and oxygenation is difficult to judge because blood gas data are rarely available in a timely fashion Furthermore, blood gases alone are poor predictors of the outcome of CPR, making their use in decisions to terminate resuscitation of questionable value The cornerstone of pH correction is adequate ventilation after effective circulation has been achieved—not NaHCO3 administration CO2 in mixed venous blood returned to the lung during CPR freely diffuses into the airway for elimination; however, reductions in pulmonary blood flow profoundly limit the capacity for CO2 excretion Consequently, hypocapnia seldom is produced at the tissue level during ongoing CPR Conversely, excessive NaHCO3 administration can produce hyperosmolality and paradoxical cellular acidosis Because exhaled CO2 measurements reflect the effectiveness of the circulation during CPR, they predict efficiency of compressions as well as outcome Higher endtidal levels of CO2 (>10 mm Hg) indicate improved perfusion and portend a better prognosis, whereas persistently low end-tidal CO2 concentrations (