Venous Return and Shock

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OVERVIEW

“Obviously, except under momentary conditions the venous return and the cardiac output must be equal.” — Arthur Guyton

STARLING’S LAW

  • By raising or lowering an artificial venous reservoir, Starling showed that increased right atrial pressure resulted in increased stroke volume
  • This resulted in Starling’s law: ventricular muscle contracts with greater force when stretched
  • This serves to ensure that the heart pumps out out whatever volume is delivered to it (unless heart failure supervenes due to excess ventricular stretch or impaired contractility)
  • Changes in venous return cause the ventricle to move along a single Frank-Starling curve that is defined by the existing conditions of afterload and inotropy and diastolic compliance
  • stroke volume is not governed by venous return (the flow of blood) and is not controlled by the ventricles or Starling’s Law, but by atrial stretch

GUYTON’S MODEL

According to the Guyton model cardiac output is determined by the interaction of cardiac function and venous return function (as shown by Guyton’s curves)

  • Guyton proposed that two key characteristics of the peripheral circulation determine cardiac output: right atrial pressure (RAP) and ‘mean circulatory filling pressure’ (MCFP)
  • The volume filling the compliant vessels of the vasculature provides an elastic recoil pressure, which is the major source of energy for the flow of blood to the right heart
  • The Guyton model has been criticised as the curves place RAP on the x-axis and flow on the y-axis, implying that RAP was actually the independent variable launched the (Pms−Pra)/Rven concept.

Venous return function and mean filling pressures

  • RAP acts as a backpressure to this flow, the driving pressure is mean circulatory filling pressure (MCFP)
  • MCFP represents the average integrated pressure throughout the circulatory system — it can be measured by stopping blood flow and allowing the pressures throughout the circulatory system to reach equilibriu
  • MCFP may be thought of as a measure of the elastic recoil potential stored in the walls of the entire circulatory system (including the heart and pulmonary circulation) — it is a function of the volume of fluid within the system and the capacitance of the system
  • Mean systemicfilling pressure (MSFP), is different to MCFP, it represents the pressure generated by elastic recoil in the systemic circulation during a no-flow state
  • resistance and capacitance at the organ and muscle are the main determinants of MCFP

Cardiac function

  • increasing blood volume, with a concomitant rise in RAP and atrial stretch, is the prime factor determining cardiac output
  • the heart can regulate cardiac output by regulating RAP — RAP determines SV by causing atrial stretch, promoting delivery of blood to the ventricle
  • The heart also restores the volume that drains from the systemic circulation and maintains MSFP

DIFFERENCES BETWEEN THE ARTERIAL AND VENOUS CIRCULATIONS

Arterial circulation

  • The arterial system’s function is to distribute blood
  • its immediate goal of maintaining arterial pressure is a guarantee that any tissue receives the blood that it requires through local vasodilatation
  • governed by laws of pressure difference (MAP = CO x SVR) analogous to Ohm’s law (V = I.R)
  • arterial tone is analogous to electrical resistance, an increase leads to decreased cardiac output (unless other compensatory factors intervene)

Venous circulation

  • The venous system’s function is to collect blood
  • sometimes conceived as analgous to the arterial circulation (MSFP – RAP = CO x venous resistance)
  • however, veins are predominantly capacitance vessels
  • Venules and veins contain ∼70% of blood volume at a low pressure
  • more meaningful for the venous circulation is the equation P = V / C; P = pressure, C = volume and C = venous capacitance (whereas the capacitance of the arterial circulation can largely be ignored)
  • like electrical capacitors, where voltage is proportional to charge, pressure is proportional to volume
  • increased venous tone primarily affects capacity, volume is primarily regulated not tone

REGULATION OF VENOUS RETURN

  • best thought of as control of venous capacitance
  • resistance plays little role in affecting flow from the venous capacitance vessels to the heart, except in situations such as positive pressure ventilation
  • cardiac output is not control by flow (venous return) — they are equivalent, except momentarily — instead cardiac output is control by volume (venous cpacitance) which determines RAP (leading to atrial stretch)
  • any difference between VR and CO leads to an altered venous accumulation rate which in turn leads to venous excess, a volume of blood in the venous circulation that does not enter the arterial circulation, and changes in right atrial pressure
  • sympathetic venoconstriction is profound regulators of venous return/ cardiac output; even the stress of mental arithmetic can cause a significant decrease in venous capacitance!

References and Links

Journal articles

  • Funk DJ, Jacobsohn E, Kumar A. The role of venous return in critical illness and shock-part I: physiology. Crit Care Med. 2013 Jan;41(1):255-62. doi: 10.1097/CCM.0b013e3182772ab6. PubMed PMID: 23269130.
  • Funk DJ, Jacobsohn E, Kumar A. Role of the venous return in critical illness and shock: part II-shock and mechanical ventilation. Crit Care Med. 2013 Feb;41(2):573-9. doi: 10.1097/CCM.0b013e31827bfc25. Review. PubMed PMID: 23263572.
  • Guyton AC. Regulation of cardiac output. Anesthesiology. 1968 Mar-Apr;29(2):314-26. PubMed PMID: 5635884. [Free Full Text]
  • Reddi BA, Carpenter RH. Venous return: cardiomythology? Clin Med. 2007 Jan-Feb;7(1):35-6. Review. PubMed PMID: 17348572.
  • Reddi BA, Carpenter RH. Venous excess: a new approach to cardiovascular control and its teaching. J Appl Physiol (1985). 2005 Jan;98(1):356-64. Epub 2004 Aug 20. PubMed PMID: 15322065. [Free Full Text]

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

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