1. Elevated lactate levels suggest tissue hypoperfusion, and normal lactate clearance issuggestive of adequate fluid resuscitation.2. Always assume that even a single episode of hypotension in a trauma patient is due tobleeding, and proceed accordingly.3. Good cardiopulmonary resuscitation can make a difference for a successful resuscitationfrom cardiac arrest. Know and perform it well.4. Time to defibrillation is the most important factor in a return of spontaneous circulationfrom ventricular tachycardia and/or ventricular fibrillation.5. Pulse oximetry is good for continuous monitoring, but arterial blood gases (ABGs) arebest for diagnosis and acute management. If oximetry does not fit the clinical picture,obtain an ABG.6. Use the alveolar gas equation to help understand mechanisms of hypoxemia.7. Hemodynamic monitoring assesses whether the circulatory system has adequateperformance to supply oxygen and sustain the “fire of life.” Monitoring provides data toguide therapy but is not therapeutic.8. There is no proved benefit to colloid over crystalloid in acute resuscitation.9. Starting enteral nutrition early in critically ill patients increased survival.10. Enteral feeding in patients with shock is acceptable after the patient is resuscitated andhemodynamically stable, even if the patient is receiving stable lower doses ofvasopressors.11. The primary indications for mechanical ventilation are inadequate oxygenation, inadequateventilation, and elevated work of breathing.12. Low tidal volume mechanical ventilation can lead to improved outcomes in the patient withacute respiratory distress syndrome.13. Daily weaning assessments improve patient outcomes.14. The rate of central venous catheter–related bloodstream infections can be reduced througha combination of the use of maximal sterile barrier precautions, 2% chlorhexidine-basedantiseptic, centralization of line insertion supplies, and daily evaluation of the need forcontinued central access.15. Subclavian venous catheters have the lowest risk of bloodstream infection.16. Lung sliding on ultrasound examination effectively rules out pneumothorax at the site ofthe transducer.17. Extracorporeal membrane oxygenation can be used successfully in patients withrespiratory failure in whom low tidal volume ventilation is failing.18. Nonrecognition of an esophageal intubation leads to death; direct visual confirmationor detection of carbon dioxide must be done to confirm the proper location of anendotracheal tube.19. If a tracheostomy tube falls out of its stoma within the first 1 to 5 days of placement, do notattempt to reinsert it blindly. Perform translaryngeal intubation instead because blindattempts at reinsertion misplace the tube into a paratracheal track, compress the trachea,and cause asphyxia.20. Any airway or stomal bleeding that develops more than 48 hours after tracheotomy shouldsuggest the possibility of a tracheoarterial fistula, which develops as a communicationbetween the trachea and a major intrathoracic artery.21. A retrospective study showed that positive pressure ventilation (PPV) does not influencethe rate of recurrent pneumothorax or chest tube placements after removal. Consequently,presence of mechanical PPV is not an indication to leave a chest tube in place.22. Chest physiotherapy appears to be as effective as bronchoscopy in treating atelectasis,although bronchoscopy has a role in retained, inspissated secretions or foreign bodies.23. Pulmonary artery line placement in patients with a newly implanted (less than 3 months)implantable cardioverter defibrillator or pacemaker is associated with high risk of leaddislodgment, especially if there is a coronary sinus lead.24. Intraaortic balloon pumps should be considered in patients who may benefit fromincreased diastolic pressures (persistent refractory angina, cardiovascular compromisefrom myocardial ischemia/infarction) or decreased afterload (acute mitral regurgitation,cardiogenic shock).25. Clinical judgment should supplement severity of illness scores in defining patients withsevere community-acquired pneumonia. 26. The use of clinical criteria alone will lead to the overdiagnosis of ventilator-associatedpneumonia.27. A normal PCO2 in acute asthma is a warning sign of impending respiratory failure.28. Noninvasive mechanical ventilation reduces the need for intubation in patients with achronic obstructive pulmonary disease exacerbation and impending respiratory failure.29. Chronic hypoxemia is the most common cause of pulmonary hypertension.30. Patients with acute lung injury and acute respiratory distress syndrome die of multiorgandysfunction far more frequently than they do of refractory hypoxemia.31. For most patients, bronchial artery embolization is the treatment of choice to stophemorrhaging in massive hemoptysis.32. Because death from massive hemoptysis is more commonly caused by asphyxiation thanexsanguination, it is important to emergently maintain airway patency and protect thenonbleeding lung.33. Deep venous thrombosis and pulmonary embolism are common and oftenunderdiagnosed in critically ill patients.34. The key to treating heart failure is determining the cause, that is, reduced ejection fraction,normal/preserved ejection fraction, restrictive cardiomyopathy, hypertrophiccardiomyopathy, or right ventricular failure.35. The best clinical guide to help in choosing which treatment is appropriate for the critically illpatient with heart failure is to assess volume and perfusion status.36. Acute myocardial infarction, complicated by out-of-hospital cardiac arrest, has a very highmortality, and hypothermia may improve chances for survival and neurologic recovery.37. It is important to distinguish hemodynamically unstable arrhythmias that need immediatecardioversion/defibrillation from other more stable rhythms.38. When managing acute aortic dissection, adequate beta blockade must be establishedbefore the initiation of nitroprusside to prevent propagation of the dissection from a reflexincrease in cardiac output.39. Pulsus paradoxus is when there is respiratory variation on arterial waveform seen duringpericardial tamponade of >10 mm Hg.40. Severe sepsis ¼ sepsis plus acute organ dysfunction.41. Early diagnosis and therapeutic interventions in patients with severe sepsis or septic shockare associated with better outcomes.42. Between 60% and 80% of cases of endocarditis result from streptococcal infection.Staphylococcus aureus tends to be the most common etiologic agent of infectiveendocarditis in intravenous (IV) drug users.43. Streptococcus pneumoniae remains the most common cause of community-acquiredbacterial meningitis, and treatment directed to this should be included in the initial empiricregimen.44. Most patients do not require computed tomographic scan before lumbar puncture;however, signs and symptoms that suggest elevated intracranial pressure should promptimaging. These include new-onset neurologic deficits, new-onset seizure, and papilledema.Severe cognitive impairment and immune compromise are also conditions that warrantconsideration for imaging.45. If you suspect disseminated fungal infection, do not wait for cultures to treat.46. Reducing multidrug-resistant bacteria can only be accomplished by using fewerantibiotics, not more.47. Clinical or laboratory identification of an unusual pathogen (i.e., anthrax, smallpox, plague)should raise suspicion for a biologic attack.48. Pain disproportionate to physical findings; skin changes including hemorrhage, sloughing, oranesthesia; rapid progression; crepitus; edema beyond the margin of erythema; and systemicinvolvement should prompt intense investigation for deep infection and involvement ofsurgical consultants as needed in the case of necrotizing fasciitis or gas gangrene.49. During influenza season all persons admitted to the intensive care unit (ICU) withrespiratory illness should be presumed to have influenza and be tested and treated.50. Asplenic individuals are at risk for infection with encapsulated organism. 51. The greatest degree of immunosuppression in solid organ transplant recipients is in the 1to 6 months after transplantation.52. Severe hypertension in absence of end organ damage can be safely treated outsidethe setting of intensive care and reduction in blood pressure be achieved gently overhours to days.53. The serum creatinine level may not change much during acute renal failure in patients withdecreased muscle mass.54. In the analysis of acid-base disorders, a normal serum pH does not imply that there is notan acid-base disorder; rather it points to mixed disorder.55. Serum magnesium level should be checked and corrected, if low, in patients with refractoryhypokalemia.56. Overly rapid correction of hyponatremia or hypernatremia can result in devastatinglong-term neurologic sequelae.57. If a patient has neurologic symptoms associated with hyponatremia, one of the immediategoals of therapy should be correction of serum sodium to a safe level.58. Be systematic in your workup of gastrointestinal tract bleeding. Follow an algorithm.59. In a patient with acute pancreatitis, make sure the patient’s fluid is replenished with anadequate amount of IV fluid. This is as important as, if not more important than, the otherfacets of treatment, including pain control, nutritional support, correcting electrolyteabnormalities, treating infection (if present), and treating the underlying cause.60. Steroids should be considered for the treatment of severe alcoholic hepatitis as defined bya Maddrey’s discriminate score 32.61. Abdominal compartment syndrome is an underappreciated diagnosis.62. This is no secret—we all share the responsibility for reducing nosocomial infections.63. Worsening confusion or a new impairment in mental state during treatment of diabeticketoacidosis or hyperosmolar hyperglycemic state is life-threatening cerebral edema untilproved otherwise.64. Administering insulin without adequate fluid replacement during treatment of diabeticketoacidosis or hyperosmolar hyperglycemic state can lead to profound hypotension,shock, or cardiovascular collapse.65. An IV insulin infusion is the safest and most effective way to treat hyperglycemia in criticallyill patients.66. If the blood pressure of an ICU patient with septic shock responds poorly to repeated fluidboluses and vasopressors, hydrocortisone should be given regardless of cortisol levels.67. In most cases you do not need to treat nonthyroidal illness syndrome with levothyroxinedespite low thyroxine, triiodothyronine, and thyroid-stimulating hormone levels; insteadfollow expectantly, and recheck laboratory values in 4 to 6 weeks.68. Stable anemia is well tolerated in critically ill patients. Transfuse blood products only whennecessary or if hemoglobin level drops below 7 gm/dL.69. Although disseminated intravascular coagulation typically presents with bleeding orlaboratory abnormalities suggesting deficient hemostasis, hypercoagulability andaccelerated thrombin generation actually underlie the process.70. Surgery for cord compression can keep people ambulatory longer than radiation alone.71. For a neutropenic fever, draw cultures, give broad-spectrum antibiotics, then complete theworkup.72. In a patient in the ICU who is seen with multiorgan failure or a clinical picture resemblingfulminant sepsis, consider the diagnosis of systemic lupus erythematosus or vasculitis.73. Respiratory pattern, autonomic functions, and brain stem reflexes are critical in identifyingthe cause of coma and should be recorded in all patients.74. No ancillary test can replace an experienced clinical examination for determination of braindeath.75. The mainstay of treatment for status epilepticus includes stabilizing the patient, controllingthe seizures, and treating the underlying cause.76. ICU admission, invasive hemodynamic monitoring, and respiratory support with frequentvital capacity measurements are keys to following patients with Guillain-Barre´ syndrome.77. Tachypnea is often the first sign of respiratory muscle weakness. Respiratory musclestrength is ideally measured by maximum inspiratory flow and vital capacity (VC) inpatients with myasthenia gravis. A quick surrogate for forced VC is to ask the patient tocount to the highest number possible during one expiration.78. Benzodiazepines are the preferred agents for the treatment of alcohol withdrawal.79. Time should not be wasted pursuing radiographic confirmation when a tensionpneumothorax is suspected in a hemodynamically unstable patient. Either formal tubethoracostomy should be immediately performed or an Angiocath inserted into the secondintercostal space along the midclavicular line.80. The condition of a significant number of patients with flail chest and/or pulmonarycontusion can be safely and effectively managed without intubation by using aggressivepulmonary care, including face-mask oxygen, continuous positive airway pressure, chestphysiotherapy, and pain control.81. The model for end-stage liver disease (MELD) calculates the severity of liver disease.82. Delirium is a disturbance of consciousness with inattention, accompanied by a change incognition or perceptual disturbances that develop over a short period of time, fluctuate overdays, and remain underdiagnosed.83. Therapeutic hypothermia (temperature 30 -34 C) improves neurologic outcomes incomatose survivors of cardiac arrest.84. Heat stroke is a true medical emergency requiring immediate action: Delay in coolingincreases mortality.85. When caring for a critically ill poisoned patient, the diagnostic and therapeutic interventionsshould be started on the basis of the clinical presentation, with use of the history, thephysical examination, and recognition of toxidromes.86. Syrup of ipecac and gastric lavage have no role in the routine management of the poisonedpatient.87. Oral or IV N-acetylcysteine should be administered promptly to any patient with suspectedor confirmed acetaminophen toxicity.88. Patients with methanol and ethylene glycol ingestions present with an osmolal gap, whichcloses with metabolism and develops an anion gap acidosis. Isopropanol toxicity beginswith an osmolal gap but is not metabolized to an anion gap.89. Patients with toxic alcohol ingestion and any vision disturbance, severe metabolic acidosis,or renal failure should undergo urgent hemodialysis.90. The treatment of choice for calcium channel blocker toxicity is hyperinsulinemiaeuglycemiatherapy to maximize glucose uptake into cardiac myocytes.91. Neuroleptic malignant syndrome can occur at any age in either sex with exposure to anyantipsychotic medication.92. Although radiologic investigations and drug treatment may carry some risk of harm to thefetus, necessary tests and treatment should not be avoided in the critically ill mother.93. Patients and their families are the experts on the patient’s goals and values, and cliniciansare the experts on determining which clinical interventions are indicated to try to achievereasonable clinical goals.94. Timely ethics consultation in the ICU may mitigate conflict and reduce ICU length of stay,hospital length of stay, ventilator days, and costs.95. Only discuss treatment choices after the patient or family has been updated on medicalcondition, prognosis, and possible outcomes and once overall goals of medical care areagreed on.96. Family conferences are more successful when providers listen more and talkless. Encourage the family to discuss their understanding of illness, their emotions,and who the patient is as a person. Then respond with statements of support andunderstanding.97. All patients with impending brain death or withdrawal of care should be screened for thepossibility of organ donation.98. The gap between those patients awaiting a transplant and those donating organs iswidening exponentially—the vast majority of those on the transplant list will die waiting.99. The hospital systems investing today in advanced informatics, automated decisionanalysis, telemedicine, and/or regionalized care will be the leading systems tomorrow.100. Patient safety remains a concern in critically ill patients, and a primary barrier to improvingpatient safety is physicians’ inability to change their practice patterns.
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