Professor Leite makes two excellent points of events following a non-Hb fluid bolus - first the dilution of oxygen carrying capacity may outweigh the increase in flow thus counteracting the intended increase in oxygen flow, and second the change in viscosity lowers perfusion pressure. A LOT of events take place when infusing fluid. To name a few the rapid, unphysiological distension of the vascular bed increases MSFP with the prospect of increasing the gradient of venous return, IF the heart has the efficiency of forwarding the venous return to the pulmonary circulation and eventually the LV. Krogh is quoted writing "The heart cannot do more than send out what it gets" and you may add "if it has the efficiency to do so". Guyton described this phenomenon as "stress relaxation" of the vascular bed as a viscoelastic structure. The increase dissipated in 40 min and the initial CO was restored. The vascular bed, as well, is under the yoke of the autonomic nervous system subserving the distribution of blood between pressurizing and non-pressurizing compartment, Vs and Vu. The higher the stressed volume in a bed with constant compliance, the higher the gradient of VR and the higher CO and DO2, maybe to a level unnecessary for the aerobic metabolism of the organism. So, homeostatic reflexes in Guyton’s histocentric CV model will see to dislodging blood into unstressed volume (recall the capacitance of the splanchnic circulation). Stress relaxation and ANS are the great killjoys of the fluid response “can-can du lit” of Monnet & Teboul which is why you have to measure within the first minutes. Remains the question why we call an ambush on normal physiology for “fluid responsiveness”?
Fluids are infused to optimize or maximize flow, no…., btw, oxygen transport. What is optimum oxygen supply, or flow? How do you gauge oxygen consumption and how do you decide which delivery will satisfy the consumption? Shoemaker experimented with supranormal values and the patients did not fare well. We veil our ignorance in terms like “optimal/maximal oxygen delivery” and haven’t got an inkling what we are aiming for (I have a suggestion, but my colleagues haven’t).
How about entertaining an exercise in fluid kinetics? How does the extravasation relate to MAP? How does transcapillary refill relate to MAP. Where do we want our fluid to end up and for what purpose? The question is not settled by organizing an RCT on +/-albumin with no idea of utility of albumin. Likewise RCTs on trigger values of hemoglobin are useless as long as you don’t realize that blood means volume and not just a condiment added to the soup and that it serves a purpose that can be checked POCT: does it add to a well indicated increase in oxygen delivery?
The procedure of assessing fluid responsiveness is a magnificent demonstration of stimulus-response in an extremely complex system – like smashing a wrecking ball into a house, simultaneously trying to read the Swiss clock on the mantelpiece. Elsewhere in medical diagnostics we prefer to read a variable during stable conditions – CO, SpO2, glucose, energy expenditure – and methods for assessing the intricate variables of the CV system without interference are in existence and freely available (..and it is not Russel’s A Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation, which is just more of the same misery).
The validation procedure of the dynamic index PLR is a chapter in itself: a fluid bolus of undetermined type and volume is infused in an undetermined passage of time and status as responder or non-responder is assigned on the basis of increase of CO. This status and dichotomy are harmonized with the percentage increase engendered by a PLR through ROC analysis. A cut-off value is the result above which future patients may benefit from a similar fluid bolus. Uniformly, validation studies in PPV, SVV and PLR have produced Gaussian distributions of cut-offs reaching from 2 to 25%, pick and choose in your clinical work!
The fundamental problem is the Starling-based model which derives its fascination from the fact that clinicians associate the function curve with left sided cardiac events. In the meantime, the drama is played out on the right side which Guyton effectively pointed out mid last century. His heritage has been taken up by Parkin & Leaning, well worth a visit.
Your patient with the open chest and pus around the heart who then bled from his atrium was obviously dying! You did him a diservice by giving him fluids - you should have given him a very large dose of morphine! Otherwise the points you make are fair - but you fail to emphasize that a bleeding patient needs blood! Only a fool would wait to transfuse at a Hb of 7G/dL in a shocked patient! Even in septic shock, providing the patient is not bleeding, red cells will stay in the circulation! Similarly, in a shocked septic patient with an albumin of 15G/L, I think you would be crazy to give such a patient another crytalloid fluid bolus! And for goodness sake, measure the CVP!
How are you able to say with confidence that a fluid bolus will always decrease viscosity to the same degree it increases cardiac output?
I think there are degrees to everything. There are septic patients with true hypovolemia who do manage to sustain an improved MAP. There are also patients who are perpetually “fluid responsive” (therefore not actually) given the pathology involved in septic shock.
Fluid responsiveness does seem to be a reasonable goal in cardiogenic shock.
Well, I am confident because in order to increase cardiac output, extra fluid has to be in the vascular beds, diluting the blood.
I would be very careful in assuming any fluid-responsive septic patient is hypovolemic or in need of fluids, because every normal human being is fluid responsive all the time. It is not something to be "corrected" by fluid infusion. However, if I have reasons to believe a septic patient is hypovolemic or dehydrated, I surely infuse some amount of crystalloids. In this case I don't aim at increasing CO. I would use lack of fluid responsiveness to contraindicate further infusions.
Regarding cardiogenic shock, if you meant that a reasonable goal is restoring fluid responsiveness, I agree with you.
Completely agree. I almost don't prescribe fluids to septic-shocked patients anymore. In case I felt the need to, my decision is based on the time since the onset of the event and the likelihood of harm from fluid therapy.
I think the real inconsistency is that we know we can increase DO2 a la Rivers with oxygen, red cells and dobutamine. We don’t do it because it doesn’t work, yet we still teach this DO2 equation and use it as a justification for other treatments.
I agree he was dying. We have just talked to him so it was a hard moment. We couldn’t help ourselves.
I totally agree with your remarks. My goal is having rumors saying I give to much blood and albumin 😅. I use to talk about CVP to residents and how it correlates perfectly with inferior vena cava diameter etc. They paralyze for a few moments after hearing it. I have a draft about this correlation. One day I will be brave enough to publish it 😅
But you see, I am writing chronicles. I must leave some clues and a few loose ends…
I agree with both of you. My take is that we mistake supportive measures (vasopressors, dobutamine) for treatments. Septic patients are not dying of “lack of fluids”, hence no one will survive because you gave fluids. This is largely ignored.
Professor Leite makes two excellent points of events following a non-Hb fluid bolus - first the dilution of oxygen carrying capacity may outweigh the increase in flow thus counteracting the intended increase in oxygen flow, and second the change in viscosity lowers perfusion pressure. A LOT of events take place when infusing fluid. To name a few the rapid, unphysiological distension of the vascular bed increases MSFP with the prospect of increasing the gradient of venous return, IF the heart has the efficiency of forwarding the venous return to the pulmonary circulation and eventually the LV. Krogh is quoted writing "The heart cannot do more than send out what it gets" and you may add "if it has the efficiency to do so". Guyton described this phenomenon as "stress relaxation" of the vascular bed as a viscoelastic structure. The increase dissipated in 40 min and the initial CO was restored. The vascular bed, as well, is under the yoke of the autonomic nervous system subserving the distribution of blood between pressurizing and non-pressurizing compartment, Vs and Vu. The higher the stressed volume in a bed with constant compliance, the higher the gradient of VR and the higher CO and DO2, maybe to a level unnecessary for the aerobic metabolism of the organism. So, homeostatic reflexes in Guyton’s histocentric CV model will see to dislodging blood into unstressed volume (recall the capacitance of the splanchnic circulation). Stress relaxation and ANS are the great killjoys of the fluid response “can-can du lit” of Monnet & Teboul which is why you have to measure within the first minutes. Remains the question why we call an ambush on normal physiology for “fluid responsiveness”?
Fluids are infused to optimize or maximize flow, no…., btw, oxygen transport. What is optimum oxygen supply, or flow? How do you gauge oxygen consumption and how do you decide which delivery will satisfy the consumption? Shoemaker experimented with supranormal values and the patients did not fare well. We veil our ignorance in terms like “optimal/maximal oxygen delivery” and haven’t got an inkling what we are aiming for (I have a suggestion, but my colleagues haven’t).
How about entertaining an exercise in fluid kinetics? How does the extravasation relate to MAP? How does transcapillary refill relate to MAP. Where do we want our fluid to end up and for what purpose? The question is not settled by organizing an RCT on +/-albumin with no idea of utility of albumin. Likewise RCTs on trigger values of hemoglobin are useless as long as you don’t realize that blood means volume and not just a condiment added to the soup and that it serves a purpose that can be checked POCT: does it add to a well indicated increase in oxygen delivery?
The procedure of assessing fluid responsiveness is a magnificent demonstration of stimulus-response in an extremely complex system – like smashing a wrecking ball into a house, simultaneously trying to read the Swiss clock on the mantelpiece. Elsewhere in medical diagnostics we prefer to read a variable during stable conditions – CO, SpO2, glucose, energy expenditure – and methods for assessing the intricate variables of the CV system without interference are in existence and freely available (..and it is not Russel’s A Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation, which is just more of the same misery).
The validation procedure of the dynamic index PLR is a chapter in itself: a fluid bolus of undetermined type and volume is infused in an undetermined passage of time and status as responder or non-responder is assigned on the basis of increase of CO. This status and dichotomy are harmonized with the percentage increase engendered by a PLR through ROC analysis. A cut-off value is the result above which future patients may benefit from a similar fluid bolus. Uniformly, validation studies in PPV, SVV and PLR have produced Gaussian distributions of cut-offs reaching from 2 to 25%, pick and choose in your clinical work!
The fundamental problem is the Starling-based model which derives its fascination from the fact that clinicians associate the function curve with left sided cardiac events. In the meantime, the drama is played out on the right side which Guyton effectively pointed out mid last century. His heritage has been taken up by Parkin & Leaning, well worth a visit.
Søren Søndergaard, Silkeborg, Danmark
Your patient with the open chest and pus around the heart who then bled from his atrium was obviously dying! You did him a diservice by giving him fluids - you should have given him a very large dose of morphine! Otherwise the points you make are fair - but you fail to emphasize that a bleeding patient needs blood! Only a fool would wait to transfuse at a Hb of 7G/dL in a shocked patient! Even in septic shock, providing the patient is not bleeding, red cells will stay in the circulation! Similarly, in a shocked septic patient with an albumin of 15G/L, I think you would be crazy to give such a patient another crytalloid fluid bolus! And for goodness sake, measure the CVP!
How are you able to say with confidence that a fluid bolus will always decrease viscosity to the same degree it increases cardiac output?
I think there are degrees to everything. There are septic patients with true hypovolemia who do manage to sustain an improved MAP. There are also patients who are perpetually “fluid responsive” (therefore not actually) given the pathology involved in septic shock.
Fluid responsiveness does seem to be a reasonable goal in cardiogenic shock.
Hi Suneal thanks for commenting.
Well, I am confident because in order to increase cardiac output, extra fluid has to be in the vascular beds, diluting the blood.
I would be very careful in assuming any fluid-responsive septic patient is hypovolemic or in need of fluids, because every normal human being is fluid responsive all the time. It is not something to be "corrected" by fluid infusion. However, if I have reasons to believe a septic patient is hypovolemic or dehydrated, I surely infuse some amount of crystalloids. In this case I don't aim at increasing CO. I would use lack of fluid responsiveness to contraindicate further infusions.
Regarding cardiogenic shock, if you meant that a reasonable goal is restoring fluid responsiveness, I agree with you.
Best,
Completely agree. I almost don't prescribe fluids to septic-shocked patients anymore. In case I felt the need to, my decision is based on the time since the onset of the event and the likelihood of harm from fluid therapy.
I think the real inconsistency is that we know we can increase DO2 a la Rivers with oxygen, red cells and dobutamine. We don’t do it because it doesn’t work, yet we still teach this DO2 equation and use it as a justification for other treatments.
We are twin souls, David!
I agree he was dying. We have just talked to him so it was a hard moment. We couldn’t help ourselves.
I totally agree with your remarks. My goal is having rumors saying I give to much blood and albumin 😅. I use to talk about CVP to residents and how it correlates perfectly with inferior vena cava diameter etc. They paralyze for a few moments after hearing it. I have a draft about this correlation. One day I will be brave enough to publish it 😅
But you see, I am writing chronicles. I must leave some clues and a few loose ends…
I agree with both of you. My take is that we mistake supportive measures (vasopressors, dobutamine) for treatments. Septic patients are not dying of “lack of fluids”, hence no one will survive because you gave fluids. This is largely ignored.