The TRICC Trial. Almost every day we're asked to transfuse someone when they dip below the '10/30' mark. This dated recommendation came from a paper in 1942 and still haunts even the most storied of medical centers. Sadly, except for highly selected patient group (active MI, sepsis with low SVO2, etc.) there is not a bit of evidence, retrospective or otherwise, that says it is beneficial. In fact, volumes of retrospective papers have found that number to be too high and transfusing to meet it leads to prolonged hospital stay, increased infections rates and worsening mortality. Goal directed therapy (i.e. optimizing perfusion) is a better target than arbitrary numbers. To do that well, we need way more data. Sadly, the only major, well-conducted study on the issue in adults has been the TRICC trial. (There are several small RTCs with varying results, but in most of those the restrictive group was similar to the liberal strategy of the TRICC trial!) Two others major trials are apparently due out in the next 12 months.
What is the TRICC trial? Transfusion Requirements in Critical Care trial was run by a consortium of Canadian ICU's. The trial looked at a big, mixed group (over 800 patients w/ARDS, trauma, head injury, GI, heart disease, sepsis, etc) of anemic ICU patients and randomized them to a liberal (transfuse when hbg < 9) or conservative strategy (transfuse when hbg <7). In hospital mortality was cut by a 20% in the conservative group (p<0.05). In those that were less sick and in those under 55, conservative strategies cut the mortality rate by half (p<0.02)!
What about coronary artery disease? Retrospective analysis have found that anemic patients with active, unstable myocardial ischemia do worse, and the TRICC trial did not have enough patients in this group to make any statements one way or another. However, it did say, "there were no significant differences in 30-day mortality between treatment groups in the subgroup of patients with a primary or secondary diagnosis of cardiac disease (20.5 percent in the restrictive-strategy group and 22.9 percent in the liberal-strategy group; 95 percent confidence interval for the difference, ¡6.7 to 11.3 percent; P=0.69)." This suggest that, unless the patient has active ischemia, patients with a history of stable coronary artery disease can be safely treated like those without CAD.
Note the same group basically repeated the TRICC trial in kids - it showed about the same thing - that a conservative transfusion strategy is at least as good.
Adams RC, Lundy JS: Anesthesia in cases of poor surgical risk. Some suggestions for decreasing the risk. Surg Gynecol Obstet 1942, 74:1011-1019.
Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. N Engl J Med 1999;340:409-417[Erratum, N Engl J Med 1999;340:1056.]
Lacroix, J, Hebert, PC, Hutchison, JS, et al Transfusion strategies for patients in pediatric intensive care units. Pediatric Acute Lung Injury and Sepsis Investigators Network. N Engl J Med 2007;356,1609-1619
From Scott:
ACE Inhibitors in Acute Decompensated Heart Failure. There is question whether or not ACEI have a place in acute decompensation in heart failure. This is complicated by the fact that these drugs are a mainstay of chronic systolic heart failure therapy.
The use of ACEI in ADHF depends largely on whether or not the patient is already taking ACEI chronically. For patients that are already taking ACEI, they should be cautiously continued in the setting of ADHF in the absence of hemodynamic instability or contraindications. They should be DISCONTINUED in the following settings: Hypotension, Acute Renal Failure and Hyperkalemia.
Currently, using ACEI and ARBs in the acute setting of ADHF is not recommended. While there are some studies advocating the use of these, the recommendations I found opted against their use for several reasons:
ACEI are great drugs in chronic heart failure, preventing many long term physiologic changes in the myocardium, but are not great drugs in ADHF. The evidence I found recommends sticking to mainstays of therapy: Supplemental O2, Diuresis with a loop diuretic, Vasodilator therapy in patients without hypotension, and potential ionotrope therapy.
Colucci, WS. Gottlieb, SS, et al. Treatment of Acute Decompensated Heart Failure: Components of Therapy. UpToDate.com, Updated May 30, 2010. Copyright 2010 UpToDate.
Heart Failure Society of America. Evaluation and management of patients with acute decompensated heart failure. J Card Fail 2006; 12:e86.
From Patrick:
Basic measurements from a Swan-Ganz and what they mean.
Cardiac output is derived from PAC thermodilution method (10ml cold H2O @ a known temp is injected through a proximal thermistor port and temp is measured again at the distal port 6-10cm downstream). Faster temperature change = high CO, slower temperature change = low CO.
There are multiple methods to calculate CO, each with its own advantages / disadvantages, including: Fick principle, Finapres methodology, Dilution method, Ultrasound dilution method, Doppler ultrasound method, Pulse pressure method, MRI.
Cardiac Index = CO / BSA = (SV * HR) / BSA. Cardiac index is basically the cardiac output (CO) in relation to the body surface area (BSA), thus normalizing cardiac output to the size of the individual. Normal values are 2.6-4.2 L/min/m2. CI below 1.8L/min/m2 is indicative of cardiogenic shock. (BSA is derived from various formulas that are available, the most commonly used being the formula of DuBois and DuBois: BSA = (W^0.425 x H^0.725) x 0.007184.)
PA Pressure is directly measured through the catheter. Normal PA pressure is about 25-systolic / 10-diastolic with a mean of 15mmHg. Higher PA pressures of course indicate pulmonary hypertension.
SvO2 or mixed venous oxygen saturation should be measured in the pulmonary artery, where IVC, SVC and coronary sinus blood have mixed. This can be sampled from blood asiparated from a PA catherter or fiber-optic based probes allow for direct measurement of oxygen
saturation of the ventricular tissues. SvO2 = SaO2 - [VO2 / (1.36 x Hb x CO)]. If SaO2, oxygen consumption (VO2) and Hb remain stable, the SvO2 can be used as an indirect indicator of cardiac output. Otherwise, an increase in oxygen consumption, decrease in Hb, CO and
arterial oxygenation (SaO2) will result in a decreased SvO2.
Controversy surrounds the use of PAC and the outcomes of critically ill patients undergoing PAC monitoring. Some studies have shown reduction in mortality, while others have shown an increase in mortality. A large RCT suggested that addition of a pulmonary artery catheter (Swan-Ganz) in 433 CHF patients did not affect overall mortality and hospitalization in comparison to careful clinical assessment (ESCAPE trial). Similar neutrality of harm/benefit with PAC use was seen in critically ill patients (3). More prospective RCT are recommended to define the role of PAC in the critically ill, although it continues to be an established way of monitoring the hemodynamics in such patients (4). See attached article for more information.
Du Bois & Du Bois,Arch Intern Med 1916, 17:863
The ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation Study of Congestive Heart Failure and Pulmonary Artery
Catheterization Effectiveness. JAMA. 2005;294:1625-1633.
Shah MR, Hasselblad V, Stevenson LW, Binanay C, O'Connor CM, Sopko G, Califf, RM. Impact of the Pulmonary Artery Catheter in Critically Ill Patients. JAMA. 2005;294:1664-1670
Mathews L, Singh RKK. Swan-Ganz Catheter in Hemodynamic Monitoring. J Anaesth Clin Pharmacol 2006; 22(4) : 335-345.
From Chris:
The APACHE II Scoring System. The Acute Physiology and Chronic Health Evaluation Scoring System (APACHE) was the first scoring system of its kind to be commonly used in ICUs. The initial system was very, very complicated. It used 34 physiologic variables and a chronic health evaluation. But, it also required a lot of time to both gather the data and do the actual calculations (no useful computers way back in the 80's). The APACHE II system is a simplification of the original formula that was published in 1985. It uses 12 physiologic markers, patient age, and a chronic health evaluation. It give you a number between 0 and 71. The idea is that you can use the same calculation to determine the "seriousness" of their illness. Additional studies have shown that it often correlates very well with patient morbidity and mortality and the number is used in a lot of other clinical calculations. A 1 point increase theoretically equates to approximately a 1% increase in mortality risk. Importantly , though it was designed as a standard measure, it does not take into account the patient's actual diagnosis. This means that, strictly speaking, you can't use the APACHE II score to compare patients across different diseases. A person with CAP and an APACHE II score of 25 has a very different mortality risk than a patient admitted for sepsis and DIC with the same APACHE score.
The original article says that, in order to be of prognostic value, the score must be combined with "an accurate description of disease."
The score can be used for prognosis, and to classify patients for research.
The 12 Physiologic parameters: Rectal temp; MAP; HR; RR, O2 delivery (ml/min) Po2; pH; NA; K; Cr; Hct; WBC. You get 0-4 points for each 1 of these based on how far you are from the normal values. Then, you add, points for age and a chronic health index score. You use a chart, or an iPhone, to do the calculations.
Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985 Oct;13(10):818-29.
Miller RD Ed. Miller's Anesthesia, 7th ed. 2009
What is the TRICC trial? Transfusion Requirements in Critical Care trial was run by a consortium of Canadian ICU's. The trial looked at a big, mixed group (over 800 patients w/ARDS, trauma, head injury, GI, heart disease, sepsis, etc) of anemic ICU patients and randomized them to a liberal (transfuse when hbg < 9) or conservative strategy (transfuse when hbg <7). In hospital mortality was cut by a 20% in the conservative group (p<0.05). In those that were less sick and in those under 55, conservative strategies cut the mortality rate by half (p<0.02)!
What about coronary artery disease? Retrospective analysis have found that anemic patients with active, unstable myocardial ischemia do worse, and the TRICC trial did not have enough patients in this group to make any statements one way or another. However, it did say, "there were no significant differences in 30-day mortality between treatment groups in the subgroup of patients with a primary or secondary diagnosis of cardiac disease (20.5 percent in the restrictive-strategy group and 22.9 percent in the liberal-strategy group; 95 percent confidence interval for the difference, ¡6.7 to 11.3 percent; P=0.69)." This suggest that, unless the patient has active ischemia, patients with a history of stable coronary artery disease can be safely treated like those without CAD.
Note the same group basically repeated the TRICC trial in kids - it showed about the same thing - that a conservative transfusion strategy is at least as good.
Adams RC, Lundy JS: Anesthesia in cases of poor surgical risk. Some suggestions for decreasing the risk. Surg Gynecol Obstet 1942, 74:1011-1019.
Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. N Engl J Med 1999;340:409-417[Erratum, N Engl J Med 1999;340:1056.]
Lacroix, J, Hebert, PC, Hutchison, JS, et al Transfusion strategies for patients in pediatric intensive care units. Pediatric Acute Lung Injury and Sepsis Investigators Network. N Engl J Med 2007;356,1609-1619
From Scott:
ACE Inhibitors in Acute Decompensated Heart Failure. There is question whether or not ACEI have a place in acute decompensation in heart failure. This is complicated by the fact that these drugs are a mainstay of chronic systolic heart failure therapy.
The use of ACEI in ADHF depends largely on whether or not the patient is already taking ACEI chronically. For patients that are already taking ACEI, they should be cautiously continued in the setting of ADHF in the absence of hemodynamic instability or contraindications. They should be DISCONTINUED in the following settings: Hypotension, Acute Renal Failure and Hyperkalemia.
Currently, using ACEI and ARBs in the acute setting of ADHF is not recommended. While there are some studies advocating the use of these, the recommendations I found opted against their use for several reasons:
- Many patients with ADHF develop hypotension and/or worsening renal function> Determining the etiology of these can be complicated by recent addition of a new ACEI. Hypotension may also be prolonged with the addition of these long-acting drugs.
- Enalaprilat in particular (an IV ACEI) can have deleterious effects during acute MI, especially during HF or aggressive diuresis. Thus, this drug should be avoided in all pts with MI, and likely those with other causes of HF.
- Aggressive diuretic therapy (frequently used in pts with acute pulmonary edema) can also increase the body's response to ACEI therapy, which may increase the risks of hypotension and renal dysfuntion.
ACEI are great drugs in chronic heart failure, preventing many long term physiologic changes in the myocardium, but are not great drugs in ADHF. The evidence I found recommends sticking to mainstays of therapy: Supplemental O2, Diuresis with a loop diuretic, Vasodilator therapy in patients without hypotension, and potential ionotrope therapy.
Colucci, WS. Gottlieb, SS, et al. Treatment of Acute Decompensated Heart Failure: Components of Therapy. UpToDate.com, Updated May 30, 2010. Copyright 2010 UpToDate.
Heart Failure Society of America. Evaluation and management of patients with acute decompensated heart failure. J Card Fail 2006; 12:e86.
From Patrick:
Basic measurements from a Swan-Ganz and what they mean.
Cardiac output is derived from PAC thermodilution method (10ml cold H2O @ a known temp is injected through a proximal thermistor port and temp is measured again at the distal port 6-10cm downstream). Faster temperature change = high CO, slower temperature change = low CO.
There are multiple methods to calculate CO, each with its own advantages / disadvantages, including: Fick principle, Finapres methodology, Dilution method, Ultrasound dilution method, Doppler ultrasound method, Pulse pressure method, MRI.
Cardiac Index = CO / BSA = (SV * HR) / BSA. Cardiac index is basically the cardiac output (CO) in relation to the body surface area (BSA), thus normalizing cardiac output to the size of the individual. Normal values are 2.6-4.2 L/min/m2. CI below 1.8L/min/m2 is indicative of cardiogenic shock. (BSA is derived from various formulas that are available, the most commonly used being the formula of DuBois and DuBois: BSA = (W^0.425 x H^0.725) x 0.007184.)
PA Pressure is directly measured through the catheter. Normal PA pressure is about 25-systolic / 10-diastolic with a mean of 15mmHg. Higher PA pressures of course indicate pulmonary hypertension.
SvO2 or mixed venous oxygen saturation should be measured in the pulmonary artery, where IVC, SVC and coronary sinus blood have mixed. This can be sampled from blood asiparated from a PA catherter or fiber-optic based probes allow for direct measurement of oxygen
saturation of the ventricular tissues. SvO2 = SaO2 - [VO2 / (1.36 x Hb x CO)]. If SaO2, oxygen consumption (VO2) and Hb remain stable, the SvO2 can be used as an indirect indicator of cardiac output. Otherwise, an increase in oxygen consumption, decrease in Hb, CO and
arterial oxygenation (SaO2) will result in a decreased SvO2.
Controversy surrounds the use of PAC and the outcomes of critically ill patients undergoing PAC monitoring. Some studies have shown reduction in mortality, while others have shown an increase in mortality. A large RCT suggested that addition of a pulmonary artery catheter (Swan-Ganz) in 433 CHF patients did not affect overall mortality and hospitalization in comparison to careful clinical assessment (ESCAPE trial). Similar neutrality of harm/benefit with PAC use was seen in critically ill patients (3). More prospective RCT are recommended to define the role of PAC in the critically ill, although it continues to be an established way of monitoring the hemodynamics in such patients (4). See attached article for more information.
Du Bois & Du Bois,Arch Intern Med 1916, 17:863
The ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation Study of Congestive Heart Failure and Pulmonary Artery
Catheterization Effectiveness. JAMA. 2005;294:1625-1633.
Shah MR, Hasselblad V, Stevenson LW, Binanay C, O'Connor CM, Sopko G, Califf, RM. Impact of the Pulmonary Artery Catheter in Critically Ill Patients. JAMA. 2005;294:1664-1670
Mathews L, Singh RKK. Swan-Ganz Catheter in Hemodynamic Monitoring. J Anaesth Clin Pharmacol 2006; 22(4) : 335-345.
From Chris:
The APACHE II Scoring System. The Acute Physiology and Chronic Health Evaluation Scoring System (APACHE) was the first scoring system of its kind to be commonly used in ICUs. The initial system was very, very complicated. It used 34 physiologic variables and a chronic health evaluation. But, it also required a lot of time to both gather the data and do the actual calculations (no useful computers way back in the 80's). The APACHE II system is a simplification of the original formula that was published in 1985. It uses 12 physiologic markers, patient age, and a chronic health evaluation. It give you a number between 0 and 71. The idea is that you can use the same calculation to determine the "seriousness" of their illness. Additional studies have shown that it often correlates very well with patient morbidity and mortality and the number is used in a lot of other clinical calculations. A 1 point increase theoretically equates to approximately a 1% increase in mortality risk. Importantly , though it was designed as a standard measure, it does not take into account the patient's actual diagnosis. This means that, strictly speaking, you can't use the APACHE II score to compare patients across different diseases. A person with CAP and an APACHE II score of 25 has a very different mortality risk than a patient admitted for sepsis and DIC with the same APACHE score.
The original article says that, in order to be of prognostic value, the score must be combined with "an accurate description of disease."
The score can be used for prognosis, and to classify patients for research.
The 12 Physiologic parameters: Rectal temp; MAP; HR; RR, O2 delivery (ml/min) Po2; pH; NA; K; Cr; Hct; WBC. You get 0-4 points for each 1 of these based on how far you are from the normal values. Then, you add, points for age and a chronic health index score. You use a chart, or an iPhone, to do the calculations.
Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985 Oct;13(10):818-29.
Miller RD Ed. Miller's Anesthesia, 7th ed. 2009
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