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Venous Return Jan Bakker [email protected] Erasmus MC University Medical Center Rotterdam • 45+ ICU beds in a 1300 bed hospital • Trauma center, Only center allowed to do all transplantations in adults and children • ECMO center (last 5 mo: 20 patients) • Admitting 2500 patients in ICU and 1000 in PACU • 70% Mechanical Ventilation • APACHE II: 20±9 Research • Circulation: 10 PhD students • Ventilation: 4 PhD students • Ethics/EOL: 2 PhD students Venous Retrun ‣Do you measure venous return in your patients? Cardiac Output ‣ Is not a physiological variable ‣ Product of Stroke Volume and Heart Rate ‣ When cardiac function is normal this is a passive variable ‣ Major determinant is the return of blood to the heart (venous return) ‣ Acute decreases are not well tolerated as compensation mechanisms are limited Main functions of the heart ‣ ‣ Keep the right atrial pressure low - facilitate venous return Equal RV-output to LV-output - Frank-Starling mechanism Starling’ Law The Starling mechanism provides the “fine tuning” to match in-flow to out-flow Consider a situation where the SV of the RV is 101 ml and that of the LV is 100 ml (1% difference). Heart rate is 70 /min In 1.5 hour the total blood volume would be in the lungs! S. Magder Regulation of CO ‣ A healthy 25 year old donates one kidney to his sister ‣ In stable conditions CO is measured before donation ‣ Following complete recovery CO is measured again under stable conditions ‣ Is the CO following the removal of one kidney higher - similar - lower than before the donation? PS! Don’t consider the compensation mechanisms in the remaining kidney heart rate? This is not easy to comprehend if one nks in a ’cardiocentric’ manner and focuses on the l-known formula learned by all physiologists: carc output ! stroke volume " heart rate. effectively accommodate changes in venous return. This conceptual framework is very helpful in explaining changes in cardiac output that occur during exercise (when metabolic activity and blood flow to skeletal muscles are increased), after eating a large meal (which increases metabolic activity and blood flow in the gastrointestinal system), and in many other physiological conditions. In each of these circumstances, cardiac pumping ability plays a relatively Distribution of cardiac output diac Output is th e Sum of Tissue an d Or gan od Flow s had shown Fig. 1 before asking this question, I bt that anyone would have had difficulty answer- FIG. 1 . Relation sh ip betw een car diac output an d per iph er al blood flow r egula- Microcirculation Pulmonary circulation CO2 CO2 production CO2 flow Expiration Organ O2 consumption Circulation O2 flow Lungs Inspiration QCO2 VO2 Dilate SV HR Recruit Vt F O2 Starling’s Law CVP Output Output Starling J. Physiol 1914 CVP RAP vs CO in exercise RAP vs CO in exercise 1 Stressed volume stressed volume unstressed volume stressed volume unstressed volume stressed volume unstressed volume Determinants of venous return ➢ RAP ➢ Vascular compliance ➢ Stressed volume ➢ Resistance to venous return ➢ Distribution of blood flow Stressed volume 5 anesthetized, hypothermic (19oC) patients 3p Thoracic arch 2p Vena caval resections Passive drainage of the RA-catheter after cardiac arrest Stressed volume 1290±296 ml 20.2±1.0 ml/kg Stressed volume is 30±17% of the total blood volume Crit Care Med 1998;26(6):1061-1064 Mean Circulatory Filling Pressure The gradient for venous return is normally very small. In this case it is only 4 mm Hg Jean-François Georger Olfa Hamzaoui Anis Chaari Julien Maizel Christian Richard Jean-Louis Teboul Restoring arterial pressure with norepinephrine improves muscle tissue oxygenation assessed by near-infrared spectroscopy in severely hypotensive septic patients Intensive Care Med (2010) 36:1882–1889 DOI 10.1007/s00134-010-2013-3 ORIGINAL 188 • 28 patients with septic shock • Fluid resuscitated Abstract Purpose: To examine Received: 18 January 2010 Norepinephrine to increase MAP>65 mm Hg of administration of • the consequences Accepted: 19 July 2010 measured and served as controls. Results: In healthy volunteers, StO2 Table online: 2 Macrocirculatory variables (mean ±on SD) in septic StO Published 6 August 2010 norepinephrine muscle tissue shockranged between 75 and 90% and StO 2 2 !patients Copyright jointly held by Springer and slopes ranged between 1.5 oxygenation in severely hypotensive recovery 95 ESICM 2010 and 3.4%/s. Administration of norseptic shock patients. Meth90 which was associated ods: This was a prospective Jean-Louis Teboul is a member of the norepinephrine Before After norepinephrine epinephrine, medical advisory board of Pulsion. with an increase in MAP from 54 ± 8 observational (introduction/increase) study conducted in a (introduction/increase) medical intensive care unit of a uni- to 77 ± 985mmHg (p \ 0.05), also p<0.05 Electronic supplementary material induced increases in CI from versity hospital. We included 28 The online version of this article SAP (mmHg) 86 ± 19 126 ± 18* 80 to 3.61 ± 1.28 L/min/ 3.14 ± 1.03 (doi:10.1007/s00134-010-2013-3) contains septic shock patients that received 2 DAP (mmHg) 38 ± 7 52 ± 8* supplementary material, which is available early volume resuscitation. All were m (p \ 0.05), in StO2 from 75 ± 9 (mmHg) 54 ± 8 eligible for receiving 77 ±norepinephrine 9* to MAP authorized users. 75 (p \ 0.05) and in StO2 to 78 ± 9% introduction of -1 Heart rate (min ) 98 ± 25 because of life-threatening 101 ± 28 hypoten- recovery slope from 1.0 ± 0.6 to norepinephrine 70 Temperature (!C) 37.5 ± 1.4 sion and low diastolic 37.5 ± 1.3 1.5 ± 0.7%/s (p \ 0.05). Concluarterial increase in the dose 2 CI (L/min/m ) 3.1 ± 1.0 pressure. Muscle 3.6tissue ± 1.3* oxygen satu- sions: Norepinephrine administraof norepinephrine 65at achieving a MAP higher GEDVI (mL/m2) 687 ± 117 ration (StO2) and 730its±changes 156* during a tion aimed than 65 mmHg in septic shock EVLWI (mL/kg) 13 ± 9 vascular occlusion 13 test ± 7were mea60 life-threatening hypopatients with SaO2 (%) 94 ± 5 sured at the level93of±the4 thenar a near-infrared spec- tension resulted in improvement of PaO ± 73 115 ± 63 J.-F. Georger ! O. Hamzaoui !122 A. Chaari ! eminence using 2 (mmHg) 55 NIRS variables measured at the level troscopy (NIRS) device. J. PaCO Maizel ! C. Richard ! J.-L. Teboul ( ) after ) before 40 ± 16 40 ± 15 2 (mmHg) Transpulmonary thermodilution car- of the thenar eminence. Service de réanimation médicale, norepinephrine norepinephrine pH 7.34 ± 0.10diac index (CI) 7.33 ± 0.10 Centre Hospitalo-Universitaire de Bicêtre, and NIRS-derived (introduction/increase) ScvO2 Publique-Hôpitaux (%) ± 9 variables were obtained 72 ± 7*before and Keywords Muscle (introduction/increase) Assistance de68 Paris, tissue oxygen EA 4046, Université Paris Sud, saturation ! Norepinephrine ! after the mean arterial pressure 78,SAP rue du Général arterial Leclerc, pressure, DAP diastolic arterial pressure, MAPSeptic Fig.shock 1 Individual values ! of the muscle tissue oxygen saturatio systolic ! Microcirculation (MAP) was increased by norepi94mean 270 Le arterial Kremlin-Bicêtre, France (StO2) before and during administration of norepinephrine in sept pressure, CI cardiac index,The GEDVI end-diaspectroscopy nephrine. baselineglobal StO2 and the Near-infrared e-mail: [email protected] stolic volume index, EVLWI extravascular lung water index,variSaO2 patients. The eight patients who had already received norepinep vascular occlusion test-derived Tel.: ?33-1-45213547 arterial oxygen saturation, PaOables pressure of oxygen of 17 healthy volunteers were in rine are represented by dotted lines. The grey cross-hatched zo Fax: ?33-1-45213551 2 partial Restoring arterial pressure with norepinephrine improves m oxygenation assessed by near-in spectroscopy in severely hypote patients % Jean-François Georger Olfa Hamzaoui Anis Chaari Julien Maizel Christian Richard Jean-Louis Teboul arterial blood, PaCO partial pressure of carbon dioxide in arterial represents the range of values of the StO measured in our group Bakker et al. Ned Tijdschr Geneeskd 1996;140:2498-2502 Rare cause of shock 17 yr old, following liver transplantation Admitted in other hospital with shock: hypovolemic? Not responding to therapy Massive amounts of vasopressors Diagnosis: obstructive shock due to compression of the inferior vena cava Rapid discontinuation of the vasopressors Uneventful recovery Importance of venous return ‣ Cardiac output is coupled to oxygen demand ‣ The primary mission of the heart is to facilitate venous return by keeping RAP low to match LV-output to the demand for oxygen delivery ‣ The determinant of venous return is the stressed volume • • Increase in unstressed volume decreases CO Increase in the resistance to venous return limit CO