Surgical Critical Care and Emergency Surgery. Группа авторов

doi: 10.1097/MCC.0000000000000336. PMID: 27467272.Bonanno FG. Hemorrhagic shock: The “physiology approach”. J Emerg Trauma Shock. 2012; 5(4):285–95. doi: 10.4103/0974‐2700.102357. PMID: 23248495; PMCID: PMC3519039.

      2 A patient in the ICU is suffering from septic shock. Using the data available from a pulmonary artery catheter or an arterial line tracing, which of the following parameters are needed in order to calculate oxygen delivery (DO2)?Pulmonary artery saturation, arterial saturation, cardiac output, oxygen consumption.Arterial pO2, pulmonary artery pO2, arterial saturation, cardiac output. Cardiac output, hemoglobin, arterial O2 saturation, arterial pO2.Stroke volume, hemoglobin, pulmonary artery pO2, arterial saturation.None of the above.Tissues attempt to extract from blood the amount of oxygen required to maintain aerobic metabolism, thus mixed‐venous O2 tension falls when O2 delivery (the product of cardiac output and arterial O2 content) becomes insufficient for tissue needs. As a primary determinant of O2 delivery, cardiac output measurements often prove helpful during selection of the appropriate ventilator settings (especially PEEP) for the patient with life‐threatening hypoxemia. Depression of venous return may nullify any beneficial effect of improved pulmonary gas exchange in tissue oxygen delivery. A rational goal of resuscitative therapy in severe sepsis and shock is to restore balance between O2 delivery and demand, and boosting cardiac output is fundamental to such an approach. Aggressive goal‐oriented resuscitation in the earliest phase of management appears to improve mortality in septic patients. The oxygen delivery equation (below) expresses oxygen delivery in terms of cardiac output multiplied by the oxygen‐carrying capacity of the blood. In order to calculate the oxygen delivery (DO2) of a patient, cardiac output, hemoglobin, SaO2, and PaO2 must be known. Answer: CMayer K, Trzeciak S, Puri NK. Assessment of the adequacy of oxygen delivery. Curr Opin Crit Care. 2016; 22(5):437–43. doi: 10.1097/MCC.0000000000000336. PMID: 27467272.

      3 For a patient in hemorrhagic shock, when trying to increase oxygen delivery, which method is the most effective?Increasing hemoglobinIncreasing preloadIncrease heart rateIncrease oxygen content in the bloodIncrease the saturation of hemoglobinThe oxygen delivery equation (below) is a function of cardiac output (HR × SV), Hgb concentration, percent hemoglobin saturation with oxygen measured by blood gas (SaO2), and percent of oxygen dissolved in the plasma itself, such that: However, this dissolved fraction of oxygen (PaO2) factors only minimally into the overall oxygen delivery formula, as denoted by the 0.003 coefficient (Choice D). As such, while the PaO2 is useful for determining various aspects of care (such as a P:F ratio in ARDS), it is essentially inconsequential in determining oxygen delivery. Typically, SaO2 (oxygen saturation from blood gas) is used to calculate CaO2. SPO2 is oxygen saturation by pulse oximeter. Regarding goals of oxygen delivery, an indexed DO2 (DO2 divided by body surface area, denoted as DO2i) of 400–600 mL/min/m2 has been shown to be associated with increased survival. The most effective way to increase oxygen delivery is by increasing hemoglobin. When going from a hemoglobin of 6–8 would result in an increase of oxygen delivery by 33%. Increasing preload may increase cardiac output by increasing stroke‐volume. It would be difficult to increase cardiac output easily by 33%. Increasing preload can often decrease PaO2 (Choice B). Increasing heart rate is typically not a strategy used to increase cardiac output (Choice C). Increasing PaO2 from 60 to 100 would only increase the saturation by 10% at the most as the saturation would only go from 90 to 100% (Choice E).Answer: ALenkin AI, Kirov MY, Kuzkov VV, Paromov KV, Smetkin AA, Lie M, Bjertnæs LJ Comparison of goal‐directed hemodynamic optimization using pulmonary artery catheter and transpulmonary thermodilution in combined valve repair: a randomized clinical trial. Crit Care Res Pract. 2012; 2012:821218. doi: 10.1155/2012/821218.Mayer K, Trzeciak S, Puri NK. Assessment of the adequacy of oxygen delivery. Curr Opin Crit Care. 2016; 22(5):437–43. doi: 10.1097/MCC.0000000000000336. PMID: 27467272.

      4 4A 36‐year‐old man following an MVC has open fractures of the bilateral lower extremities, as well as bruising across his lower abdomen and significant pain on abdominal exam. His vitals are as follows: HR 109, BP 125/95, SpO2 98% on face mask, respiratory rate 18, and he is fully oriented and cooperative on exam. What percentage of total blood volume loss do you estimate the patient has experienced?<15%15–30%30–40% >40%Blood volume loss cannot be predicted in this patientSource: Data from: Mutschler A, Nienaber U, Brockamp T, et al. A critical reappraisal of the ATLS classification of hypovolaemic shock: does it really reflect clinical reality? Resuscitation 2013,84:309–313.The patient above has a narrowed pulse pressure (but is not yet hypotensive) and is tachycardic. He does not have any signs of overt shock (he is oriented and cooperative indicating adequate cerebral perfusion). Because of his tachycardia and narrowed pulse pressure with increased diastolic pressure, this would place him in class II shock, which is defined at 15–30% loss of total blood volume. By comparison, class I hemorrhagic shock is defined by less than 15% total blood volume loss, and typically does not have any significant vital sign abnormalities except for mild tachycardia. Class III hemorrhagic shock is achieved with 30–40% total blood volume loss, and will present with tachycardia, narrowed pulse pressure, hypotension, anxiety, and confusion. Therefore, a hypotensive patient from hemorrhagic shock has lost approximately 1.5–2 L of blood. Class IV hemorrhagic shock will have greater than 40% blood volume loss and will appear similar to class III but patients are typically lethargic instead of anxious. The astute clinician should recognize hemorrhagic shock long before the onset of hypotension, as by this point significant blood loss has already occurred. Instead, narrowed pulse pressure and tachycardia should be the first vital sign changes to point toward hemorrhage.Answer: BBonanno FG. Hemorrhagic shock: The “physiology approach”. J Emerg Trauma Shock. 2012; 5(4):285–95. doi: 10.4103/0974‐2700.102357. PMID: 23248495; PMCID: PMC3519039.Table 6.1 Classes of hemorrhagic shockParameterClass IClass II (mild)Class III (moderate)Class IV (severe)Approximate blood loss<15%15–30%31–40%>40%Heart rate↔↔/↑↑↑/↑↑Blood pressure↔↔↔/↓↓Pulse pressure↔↓↓↓Respiratory rate↔↔↔/↑↑Urine output↔↔↓↓↓Glasgow Coma Scale score↔↔↓↓Base deficit^*0 to −2 mEq/L−2 to −6 mEq/L−6 to −10 mEq/L−10 mEq/L or lessNeed for blood productsMonitorPossibleYesMassive transfusion protocol* Base excess is the quantity of base (HCO3−, in mEq/L) that is above or below the normal range in the body. A negative number is called a base deficit and indicates metabolic acidosis.Lawton LD, Roncal S, Leonard E, Stack A, Dinh MM, Byrne CM, Petchell J. The utility of Advanced Trauma Life Support (ATLS) clinical shock grading in assessment of trauma. Emerg Med J. 2014; 31(5):384–9. doi: 10.1136/emermed‐2012‐201813. Epub 2013 Mar 19. PMID: 23513233.

      5 A 16‐year‐old man trapped inside a house fire was found unconscious. He suffered a large laceration to his left lower extremity from some falling debris, and was intubated in the ED due to GCS of 6. His SpO2 (from his pulse oximeter) shows 99%; however, his ABG drawn at the same time demonstrates a SaO2 (from his blood gas) of 84%. You also note that he has pink nail polish on all of his fingernails. Which of the following could be a cause for this discrepancy?Acute blood loss anemiaCarboxyhemoglobinemiaCyanide toxicityPositioning of the pulse oximeter on the patient's ear instead of his fingerNail polishBedside pulse oximetry is a cornerstone of hemodynamic monitoring in the intensive care unit due to its noninvasive nature and accuracy. However, there are multiple situations in which readings can be erroneous. Once such example is sickle cell disease, which causes deformation of hemoglobin and decreases flow through the micro circulation, and thus causes an overestimation of readings. The clinical significance of these readings is often downplayed in studies. Acute blood loss anemia, by itself, seems to have no effect on oximetry readings (Choice A). Most peripheral sensors use two wavelengths of light: those associated with oxygenated and deoxygenated hemoglobin. These light waves are in the near‐infrared spectrum as these light waves can easily pass