Post S1P care considerations

Postoperative physiology. The circulation following S1P is one of the more challenging to manage. The following should be assessed in sequence:

Flow. Blood that the heart ejects (combined cardiac output) flows to the systemic circulation and to the pulmonary circulation in parallel. Flow (abbreviated Q) to the body (Qs) and to the lungs (Qp) occurs in proportion to the relative impedance to blood flow in each of the circulations. Lesions that increase impedance to the pulmonary circulation (namely the Sano conduit; PVR is nearly always low) may decrease PBF, causing hypoxemia and dead space ventilation. Lesions that increase impedance to systemic blood flow (e.g. aortic arch obstruction, high SVR) may decrease systemic blood flow and end-organ perfusion. Assessing flow (and more importantly oxygen delivery) following S1P is one of the most challenging components to the care of patients. Our tools for assessing flow are limited. More details of assessing the circulation can be found on pages 142-145, but a few of my guiding principles re: assessing flow following S1P are as follows.

  • Pressure measurements. Generally, the job of the heart as a pump is to separate arterial and venous pressure and to create arterial pulsatility. The closer the venous pressure approximates the mean arterial pressure, the less effective the circulation. The pulsatility of the arterial pressure following S1P is vitally important. The pulse pressure should be at least 15 mmHg. (Always ensure that the line is functioning properly but never assume that this is the problem.) A pulse pressure <10 mmHg may indicate a compromized stroke volume, which could be due to (1) decreased preload (i.e. end diastolic volume) due to hypovolemia or venodilation or (2) decreased ejection due to AVV regurgitation or ventricular dysfunction. In the setting of diminished pulsatility, a venous pressure (i.e. common atrial pressure) that is <~8 mmHg (make sure to zero and level transducer) may indicate decreased preload. This may be addressed by decreasing venodilators, administering volume, or by judicious use of vasoconstrictors. If the CAP is elevated (e.g. >12 mmHg), it may indicate ventricular dysfunction (systolic or diastolic), AVV regurgitation, or anatomic decrease in venous capacitance (e.g. thrombus, tissue edema in sternal closure). If the circulation is significantly compromised in this setting, thoracic exploration may be therapeutic.
  • Waveforms. The waveform of the pulse oximeter gives an unbiased and accurate measure of the mass of hemoglobin being delivered to the tissue with each pulse. A concerning pulse plethysmogram (see page 145) is generally worrisome for compromized systemic perfusion. The statement ‘we are having trouble getting the pulseox to pick up’ should be considered among the most alarming. Similarly, a narrow (in width of the waveform, not height) arterial line waveform (even in the setting of an appropriate pulse pressure) may indicate a low stroke volume combined with a compensatorily elevated SVR. This is a similarly worrisome state to a narrow pulse pressure. CICU manual_WORKING.indd 268 1/11/21 9:26 PM 269Post S1P care considrations
  • Physical exam. Of course, the physical exam provides a vital and irreplaceable barometer of circulatory health. Skin color to experienced eyes (with the lights on) is a sensitive marker of perfusion, as centralized shunting of blood flow away from the skin to vital organs may produce pallor or gray skin. Pulse strength is also critically important to assess but takes time to master with sufficient confidence to use in clinical decision-making. Pay attention to pulse strength (and how patients subsequently do over time) in order to get good at this.
  • Metabolism. Patients with severe limitations to systemic oxygen delivery will have compromised metabolism. This can be measured as (1) the ability to maintain core body temperature, (2) the amount of CO2 produced per minute (VCO2) and (3) the amount of oxygen consumed per minute (VO2). VCO2 is measured on standard ventilators and is useful to track over time. When VCO2 or VO2 is <3 mL/kg/minute, metabolism may be compromised by a diminished circulation. Because heat is generated by metabolism (i.e. O2 consumption and CO2 production), temperature, VCO2 and VO2 are co-linear with one another.
  • SvO2. An SvO2 (venous oxyhemoglobin saturation) <30% is always concerning and is indicative of tissue hypoxia. However, an SvO2 of 30-50% in the setting of SaO2 in the 80-90% range can be similarly concerning. There are many ways that the SvO2 can be falsely reassuring in a shock state, including arterial contamination of venous blood from TR or leftward atrial shunting, PAPVR, hypothermia, even air bubbles within the sampling syringe. Note that NIRS does not correlate with SvO2 in the ranges discussed above, and an rSO2 in the 50-60’s does not ensure that the SvO2 is normal; however, a low NIRS is specific for a low SvO2.
  • Lactic acid. Serum lactic acid accumulates in the setting of anaerobic metabolism. An elevated lactic acid (>3 mmol/L) is generally concerning. Several caveats exist. Serum lactic acid may remain elevated in the absence of ongoing anaerobic metabolism in the presence of hyperglycemia since lactic acid is a component of the Cori cycle. Lactic acid may also remain elevated in the setting of hepatic dysfunction. Lactic acid may be falsely reassuring in the setting of microvascular arteriovenous shunting in shock states.

Oxygenation and ventilation. In most cases, there is complete atrial mixing, creating a common arterial saturation in the pulmonary and systemic circulation. The exception to this is the case of MS/AS in which the LV may eject purely pulmonary venous return (most oxygenated) into the aorta, which may stream towards the right hand and brachiocephalic vessels, causing a differential in saturations between the right arm and remaining extremities. Hypoxemia is most commonly caused by either pulmonary vein desaturation (intrapulmonary shunting, often responsive to hand ventilation, suctioning, increased FiO2, rarely iNO) or decreased pulmonary blood flow. Hypercarbia is an equally common manifestation of decreased pulmonary blood flow in this population. Often, decreased PBF is due to decreased total cardiac output. An approach for troubleshooting hypoxia follows.

Systemic hypoperfusion following S1P


References for S1P Outcomes

2013, ASE – Retrograde flow in BTS and RVPAS does not affect clinical outcomes

2013, Circ CV Imaing – Shunt type does not affect RV echo parameters, volume unloading following Glenn

2013, Circulation – 18% incidence of recurrent arch obstruction following S1P

2013, JTCVS – Timing and outcomes of BDG in SVR trial

2014, J Peds – Feeding practices following S1P

2016, JAHA – Digoxin reduces interstage mortality

2016, JHLT – Transplant outcomes following S1P

2017, ASE – BDG decreases RV volume and mass equally

2008, JTCVS – Mathematical modeling of DO2 in BTS vs Sano

2010, Circulation – Enalapril does not change interstage survival or growth following S1P

2010, JTCVS – Preoperative risk factors

2010, NEJM – SVR trial 2011, Ped Card – Celiac artery flow better in Sano than BTS

2012, Circulation – 14 month SVR followup

2012, Circulation – Shunt type does not impact ventricular size at 14 month

2012, JACC – Current outcomes in HLHS

2012, JTCVS – Causes and timing of death in SVR trial

2012, JTCVS – Differences in postoeperative care following S1P

2012, JTCVS – Low center volume, open sternum affect survival to hospital discharge

2012, Circulation – 14 month SVR followup

2013, Circulation – 18% incidence of recurrent arch obstruction following S1P

2011, J Peds – Factors affecting growth following S1P

2017, J Peds – WAZ is -0.5 at 6 years following S1P