Thank you a lot for this podcast. I love the way things are presented. I appreciated the modesty and the obvious expertise of Dr Suchitra Ranjit and Dr Luregn Schglapbach. I have a lot of questions. Perhaps the easiest way to formulate them is to describe our practice. In my unit, we first try to optimise the pulmonary blood flow (lung volume, PaCO2, pH, sometimes pulmonary vasodilators like milrinone or sildenafil). We consider that a better pulmonary circulation is crucial for the emptying of the right ventricule (hence optimizing venous return) and the filling of the left ventricule (increasing cardiac output). Often the pulmonary artery pressure is very high. If the blood pressure is already low or if the peripheral perfusion is compromised, we start norepinephrine (+or- an inotrope) early. We look for the need of fluid by interrogating the sus hepatic vein doppler AND the renal venous doppler RVD. A continuous RVD is suggestive that the patient is fluid responsive. Even if this is the case, we try to look for another way than giving fluids to optimise the perfusion (color of the lips, overall color of the patient, warmth of the feet, peripheral capillary refill, transcranial doppler, renal arterial doppler, SvO2). This can be by administering milrinone, dobutamine, adjusting the rate of noradrenaline or manipulating the ventilator. Fluids are given only if this measures are not effectives (as 30 min infusion under close surveillance of the RVD and pulmonary echography (looking for apparition of B lines)). For some patients we restore easily a good perfusion (clinical, arterial dopplers, SvO2 - and lactates when available). For other, we have an incomplete improvement (good diuresis, sufficient arterial pressure but still a somehow prolonged capillary refill time despite good cardiac contractility, a full fluid resuscitation and optimal pulmonary parameters). In general we give time to the patient to equilibrate or to manifest a hidden physiological derangement. This pose the question of resuscitative end points. Must we target normal parameters? My other question is since sepsis is a syndrome of organ dysfunction and septic shock is sepsis with hemodynamic perturbations, is it suffisant to address solely the circulation? What about prevention or limitation of ongoing organ dysfunction? what is the role of microcirculation (nitroglycerin at high dose, beta bloquer or alpha2 agonist after stabilisation)? Can we improve organ vitality by a better lymphatic drainage (interstitial washout)? The technique of direct peritoneal resuscitation seems to improve the outcome of multiple organ failure such a severe case as pancreatitis, poly trauma, open abdomen,...). We suspect that infusing an hypersonic dialysate divert a rich cytokine lymphatic fluid form the thoracic canal. What is also the possible rôle of fecal transplantation witch gives impressive results in a numbers of clinical reports of shock and organ failure? I am sorry to be too long, my last question is conceptual: why not to consider that septic shock is an arterial venous shunting? This my explain the high cardiac output, the "hypovolemia", the efficacy of noradrenaline, the effects of beta blockers, de non concordance of the micro and the microcirculation, the positive effets of nitroglycerin in a number of clinical reports. The actual formula for calculating systemic vascular resistance suppose a 1- continuity between the arterial and venous circulation and 2- that the left ventricule is the sole driving motor for blood from the aorta to the right atrium. The venous side seems instead disconnected for the arterial one (the so called waterfall effect). Blood flow is driven to the right cavities by the mean systemic pressure as well as by squeletic muscule contractions, mouvements of the abdominal viscera and variations in intrathoracic pressure and pulmonary volume. Theses forces are not accounted by the formula for systemic vascular resistance. So one can doubt if systemic vascular resistance are truly low in the context of septic shock. Arteriovenous shunting will give nonetheless a low systemic resistance by using the formula RVS= (MAP-RAP)/CO. I apologise for my long commentary and thank you again for this elegant and instructive podcast.
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Thank you a lot for this podcast. I love the way things are presented. I appreciated the modesty and the obvious expertise of Dr Suchitra Ranjit and Dr Luregn Schglapbach. I have a lot of questions. Perhaps the easiest way to formulate them is to describe our practice. In my unit, we first try to optimise the pulmonary blood flow (lung volume, PaCO2, pH, sometimes pulmonary vasodilators like milrinone or sildenafil). We consider that a better pulmonary circulation is crucial for the emptying of the right ventricule (hence optimizing venous return) and the filling of the left ventricule (increasing cardiac output). Often the pulmonary artery pressure is very high.
If the blood pressure is already low or if the peripheral perfusion is compromised, we start norepinephrine (+or- an inotrope) early. We look for the need of fluid by interrogating the sus hepatic vein doppler AND the renal venous doppler RVD. A continuous RVD is suggestive that the patient is fluid responsive. Even if this is the case, we try to look for another way than giving fluids to optimise the perfusion (color of the lips, overall color of the patient, warmth of the feet, peripheral capillary refill, transcranial doppler, renal arterial doppler, SvO2). This can be by administering milrinone, dobutamine, adjusting the rate of noradrenaline or manipulating the ventilator. Fluids are given only if this measures are not effectives (as 30 min infusion under close surveillance of the RVD and pulmonary echography (looking for apparition of B lines)).
For some patients we restore easily a good perfusion (clinical, arterial dopplers, SvO2 - and lactates when available). For other, we have an incomplete improvement (good diuresis, sufficient arterial pressure but still a somehow prolonged capillary refill time despite good cardiac contractility, a full fluid resuscitation and optimal pulmonary parameters). In general we give time to the patient to equilibrate or to manifest a hidden physiological derangement. This pose the question of resuscitative end points. Must we target normal parameters?
My other question is since sepsis is a syndrome of organ dysfunction and septic shock is sepsis with hemodynamic perturbations, is it suffisant to address solely the circulation? What about prevention or limitation of ongoing organ dysfunction? what is the role of microcirculation (nitroglycerin at high dose, beta bloquer or alpha2 agonist after stabilisation)? Can we improve organ vitality by a better lymphatic drainage (interstitial washout)? The technique of direct peritoneal resuscitation seems to improve the outcome of multiple organ failure such a severe case as pancreatitis, poly trauma, open abdomen,...). We suspect that infusing an hypersonic dialysate divert a rich cytokine lymphatic fluid form the thoracic canal.
What is also the possible rôle of fecal transplantation witch gives impressive results in a numbers of clinical reports of shock and organ failure?
I am sorry to be too long, my last question is conceptual: why not to consider that septic shock is an arterial venous shunting? This my explain the high cardiac output, the "hypovolemia", the efficacy of noradrenaline, the effects of beta blockers, de non concordance of the micro and the microcirculation, the positive effets of nitroglycerin in a number of clinical reports.
The actual formula for calculating systemic vascular resistance suppose a 1- continuity between the arterial and venous circulation and 2- that the left ventricule is the sole driving motor for blood from the aorta to the right atrium. The venous side seems instead disconnected for the arterial one (the so called waterfall effect). Blood flow is driven to the right cavities by the mean systemic pressure as well as by squeletic muscule contractions, mouvements of the abdominal viscera and variations in intrathoracic pressure and pulmonary volume. Theses forces are not accounted by the formula for systemic vascular resistance. So one can doubt if systemic vascular resistance are truly low in the context of septic shock. Arteriovenous shunting will give nonetheless a low systemic resistance by using the formula RVS= (MAP-RAP)/CO.
I apologise for my long commentary and thank you again for this elegant and instructive podcast.
Thank you for sharing 🇺🇸🇹🇳🇺🇸🇹🇳
Fluid can help or kill.