Background
Theoretic principles
Technical considerations
Age | Depth(mm) | Mean velocity (cm/s) | Peak systolic velocity (cm/s) | End-diastolic velocity (cm/s) |
---|---|---|---|---|
0–3 mo | 25 | 24–42+/-10 | 46–75+/-15 | 12–24+/-8 |
3–12 mo | 30 | 74 +/- 14 | 114 +/- 20 | 46+/- 9 |
1–3 yr | 35–45 | 85 +/- 10 | 124 +/- 10 | 65 +/- 11 |
3–6 yr | 40–45 | 94 +/- 10 | 147 +/- 17 | 65 +/- 9 |
6–10 yr | 45–50 | 97 +/- 9 | 143 +/- 13 | 72 +/- 9 |
10–18 yr | 45–50 | 81 +/- 11 | 129 +/- 17 | 60 +/- 8 |
Relation between blood flow velocity and cerebral blood flow
Methodology
Literature analysis
TCD and cerebral blood flow modifications (table 2)
Author [reference] | Journal (Year of Publication) | Type of study and Number of patients | Main findings |
---|---|---|---|
Lindegaard KF [4] | Stroke (1987) | Observational on 7 adult patients | Linear relationship between flow volume and blood velocity in MCA is present. |
Weyland A [5] | Anesthesiology (1994) | Observational on 15 adult patients | Linear relationship between flow volume and blood velocity in MCA is present before and after CPB but cannot reliably predict percentage changes in CBF during CPB. |
Bishop CCR [6] | Stroke (1986) | Observational on 17 adult patients | Changes in MCA velocity reliably correlate with changes with CBF evaluated with Xenon133
|
Rosemberg A [7] | Pediatric Research (1985) | Experimental in newborn lambs | Changes in cerebral blood flow velocity are useful qualitative measures of changes in cerebral blood flow |
Trivedi U [8] | Annals of Thoracic Surgery (1997) | Randomized trial on 60 adult patients receiving either α-stat or pH stat management based CPB | Measurement of MCA velocity by TCD expressed as relative changes of a pre-CPB level can be used to examine CBF changes during CPB |
Role of TCD during deep hypothermic cardio pulmonary bypass, deep hypothermic circulatory arrest and low flow cardio pulmonary bypass (table 3)
Author [reference] | Journal (Year of Publication) | Type of study and Number of patients | Main findings |
---|---|---|---|
Norwood WI [9] | Journal of Thoracic Cardiovascular Surgery (1979) | Experimental study on neonatal rats | Hypothermia during CPB reduces metabolic activity, CBF and CMRO2, so that it is possible to maintain energy stores and provide organ protection during low flow state |
Greeley WJ [10] | Journal of Thoracic Cardiovascular Surgery (1991) | Prospective study on 46 pediatric patients | DHCA changes cerebral metabolism and blood flow after the arrest period |
Fox LS [11] | Journal of Thoracic Cardiovascular Surgery (1984) | Experimental study on 9 monkeys randomly assigned to 4 perfusion flow rates varying from 0.25 to 1.75 L/min/m2
| All areas of the brain remain perfused, even at low perfusion flow rates, during profoundly hypothermic cardiopulmonary bypass, and brain oxygen consumption is maintained in part by increased oxygen extraction and in part by redistribution of the perfusate from the remaining body to the brain |
Rebeyka IM [12] | Annals of Thoracic Surgery (1987) | Experimental study on 6 dogs and prospective study on 5 patients subjected to brief periods of low-flow CPB (Q = 1.0 L/min/m2.) at 21 degrees to 25 degrees C°. | In the absence of cerebral vascular disease, the flow rate threshold for incurring functional cerebral injury during hypothermic (25 degrees C) nonpulsatile CPB is less than 1.0 L/min/m2. |
Taylor R [13] | Anesthesia Analgesia (1992) | Observational study on 25 infants and neonates | 1) Autoregulation is preserved during normothermic CPB, it begins to be altered at temperature less than 25°C, and it is lost at temperature less than 20°C. 2) A significant decrease in CPP and CBF is shown during extreme low flow CPB. |
Jonassen A [14] | Journal of Thoracic Cardiovascular Surgery (1995) | Observational on 37 pediatric patients | Detectable cerebral blood flow at pump flow rate and mean arterial pressure values of 27 mmHg (lower than those reported by Taylor). |
Greeley WJ [15] | Circulation (1989) | Observational on 67 pediatric patients | During CPB rewarming, CBF returns to baseline values, except in patients exposed to periods of DHCA where CBF remains decreased. |
Astudillo R [16] | Annals of Thoraci Surgery (1993) | Observational on 22 small children | Low cerebral perfusion immediately following DHCA is characterized by a prolonged period of absent diastolic CBFV in MCA while patients subjected to continuous low-flow perfusion technique showed a CBFV close to baseline values at skin closure. |
Rodriguez R [17] | Journal of Thoracic Cardiovascular Surgery (1995) | Randomized trial on 16 infants treated with or without 10 minutes of cold reperfusion before rewarming after DHCA. | A delay in rewarming on reperfusion after DHCA may be beneficial as demonstrated by recovery of a diastolic doppler signal. |
Zimmerman A [18] | Journal of Thoracic Cardiovascular Surgery (1997) | Observational on 28 neonates | Cerebral perfusion can be detected by TCD in the MCA in some neonates at bypass flow as low as 10 ml/kg per minute. |
Role of TCD during regional low-flow perfusion for neonatal aortic arch reconstruction (table 4)
Author [reference] | Journal (Year of Publication) | Type of study and Number of patients | Main findings |
---|---|---|---|
Pigula F [19] | Journal of Thoracic Cardiovascular Surgery (2000) | Observational on 6 neonates | Significant decreases are shown in both cerebral blood volume and oxygen saturation in children who underwent repair with DHCA as compared with children with RLFP. |
Andropulos D [20] | Journal of Thoracic Cardiovascular Surgery (2002) | Observational on 34 neonates | The use of TCD is able to maintain cerebral oxygen saturations and blood flow velocities within 10% of baseline, in order to prevent cerebral hyperperfusion during periods with high NIRS saturation values. |
Alpha versus Ph stat blood gas management (table 5)
Author [reference] | Journal (Year of Publication) | Type of study and Number of patients | Main findings |
---|---|---|---|
Trivedi U [8] | Annals of Thoracic Surgery (1997) | Randomized trial on 60 adult patients receiving either α-stat or pH stat management based CPB | A decrease of CBF (evaluated by Xenon-133 and CBFV) is shown during 28° bypass in patients subjected to α-stat management. This is associated with a significant reduction in PaCO2, while there is no reduction in patients subjected to pH-stat management. |
Patel RL [22] | European Journal of Cardiothoracic Surgery (1993) | Randomized protocol on 70 adult patient undergoing α-stat or ph stat CPB | The cerebral extraction ratio for oxygen indicated a degree of mismatch of cerebral perfusion and demand during CPB in both pH-stat and alpha-stat groups. This mismatch was more pronounced in the pH-stat group than in the alpha-stat group, indicating greater disruption in cerebral autoregulation in the former group. |
Gruber E [23] | Anesthesia Analgesia (1999) | Prospective randomized study on 35 neonates and infants managed with different hematocrit values | An inverse relation is present between hematocrit and CBFV during DHCPB |
Rodriguez R [24] | Annals of Thoracic Surgery (2000) | Observational on 124 children | Aorto-venous can impair cerebral perfusion which may be effectively followed by Doppler flow. |
Hematocrit (table 5)
Effects of cannulation for cardiopulmonary bypass (table 5)
Clinical implications
Multimodality neurological monitoring (table 6)
Author [reference] | Journal (Year of Publication) | Type of study and Number of patients | Main findings |
---|---|---|---|
Austin E III [25] | Journal of Thoracic and Cardiovascular surgery | Observational on 250 pediatric patients. | Interventions based on neurophysiologic monitoring (NIRS, TCD, EEG) decrease postoperative neurologic sequelae and reduce hospital lenght of stay. |
Andropoulos D [26] | Anesthesia Analgesia (2004) | Literature review and institutional data report | Multimodal neurological monitoring in conjunction with a treatment algorithm may improve neurological outcome. |
O'Brien [27] | Anesthesiology (1997) | Observational on 25 children | Microemboli can be detected in the carotid arteries of children during repair of congenital heart disease and are especially prevalent immediately after release of the aortic cross clamp. |
TEMPERATURE | BLOOD PRESSURE | TCD | NOTIFICATION | INTERVENTION |
---|---|---|---|---|
Prebypass
| ||||
/ | / | - peak velocity | Aorta obstructed | Adjust aortic cannula |
/ | / | - diastolic velocity | Cava obstructed | Asdjust venous cannula |
CPB
| ||||
/ | / | + peak velocity | Hyperemia | - Pump flow |
/ | / | Gas emboli | Gas emboli | Deair, repair circuit |
+ | / | - peak velocity | Flow metabolism uncoupling | +BP; - metabolic demand |
/ | / | - peak velocity | Low cerebral flow | Adjust aortic cannula/clamp; + Pump flow |
Postbypass
| ||||
/ | / | - Diastolic velocity | Cerebral edema | Mannitol; ultrafiltration |
Anytime
| ||||
/ | - | - Peak velocity | Loss of autoregolation | + BP; neuroprotection |
+ EEG frequency
| ||||
/ | /, + | /, + peak velocity | Insufficient sedation | + Sedation |