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Transmural
Pressure
= V2 - V1/P
= Vt - Vo/P
Vs
Atrium C = Vs/P
Venous (PRA)
Reservoir
Vt
Pms
Vo 0 V1 V2
A B
Pms - PRA VR
VR = slope = Pms
Rv Pms - PRA
Pms - PRA 1 = Pms - PRA Rv
so Rv =
VR slope VR
Normal
Venous Rv = 1/slope Venous
Rv
Return slope = 1/Rv Return
Pms
1/Rv
Pms
0 0
Right Atrial Pressure (PRA ) Right Atrial Pressure
contractility
afterload
Cardiac cardiac
normal compliance
Output
contractility
afterload
To provide a conceptual and clinical review of the phys- various shock states including hypovolemic, cardiogenic, obstructive,
iology of the venous system as it is related to cardiac function in and septic shock. In particular, we demonstrate how these shock
health and disease. states perturb venous return/right heart interactions. We also show
An integration of venous and cardiac physiology under nor- how compensatory mechanisms and therapeutic interventions can
mal conditions, critical illness, and resuscitation. tend to return venous return and cardiac output to appropriate values.
The usual clinical teaching of cardiac physiology focuses An improved understanding of the role of the venous
on left ventricular pathophysiology and pathology. Due to the wide ar- system in pathophysiologic conditions will allow intensivists to
ray of shock states dealt with by intensivists, an integrated approach better appreciate the complex circulatory physiology of shock
that takes into account the function of the venous system and its inter- and related therapies. This should enable improved hemodynamic
action with the right heart may be more useful. In part II of this two-part management of this disorder. (Crit Care Med 2013; 41:573579)
review, we describe the physiology of venous return and its interaction cardiogenic shock; cardiovascular physiology; hemo-
with the right heart function as it relates to mechanical ventilation and dynamics; hemorrhagic shock; obstructive shock; septic shock
M
any, if not most, clinicians approach the management and treat the common hemodynamic problems encountered
of acute cardiovascular dysfunction and shock in critical care. The key concepts described here are covered in
using an analysis that emphasizes left ventricular detail in the rst part of the review. The reader is encouraged
physiology, probably as a consequence of medical training to read that earlier physiologic review before proceeding with
that emphasizes the role of left ventricular dysfunction in this current pathophysiologic review.
ischemic heart disease, the most common cause of death in To review, only a portion of the total blood volume (Vt )
the developed world. Intensivists deal with a broader array of contributes to the pressures generated in the circulation (1
cardiovascular perturbations including shock states in which 6). The unstressed intravascular volume (Vo) can be defined
vascular dysfunction and other extracardiac perturbations as that volume required to fill the circulatory system to
may dominate the clinical picture (e.g., septic, hypovolemic, capacity without any increase in cardiovascular transmural
or obstructive shock). In the rst part of this two-part review, pressure. Stressed volume (Vs) would be that amount
we reviewed an approach to cardiovascular physiology that which, when added to the unstressed volume, generates the
incorporates both cardiac and vascular elements that may be cardiovascular transmural pressure. Passive exsanguination
more useful to intensivists than one that focuses exclusively on of an anticoagulated experimental animal would result in a
left ventricular physiology. In the second part of this review, we large blood loss. The external, exsanguinated volume would
describe various shock states and how the knowledge of venous represent the Vs. The amount remaining in the circulation
return (VR) and cardiac output (CO) curves help to diagnose would be Vo.
The mean systemic pressure (Pms) is the average pressure
1
Section of Critical Care Medicine, Department of Medicine, University of throughout the entire circulatory system (cardiac/arterial/cap-
Manitoba, Manitoba, Canada.
2
illary/venous). It is most easily measured when pressures are
Department of Anesthesiology and Perioperative Medicine, University of
Manitoba, Manitoba, Canada. equilibrated during brief cardiac standstill (2, 7). During ac-
3
Section of Critical Care Medicine, Cooper University Hospital, Cooper tive circulation, the portion of the cardiovascular circuit that
Medical School of Rowan University, Camden, NJ. has a pressure equivalent to Pms is found in the small veins/
The authors have not disclosed any potential con icts of interest venules in the splanchnic bed. Pms can therefore be considered
For information regarding this article, E-mail: akumar61@yahoo.com the upstream pressure driving VR (VR = Pms PRA/RV, where
Copyright 2013 by the Society of Critical Care Medicine and Lippincott PRA is right atrial pressure and RV is venous resistance). Another
Williams & Wilkins salient point is that the RV is represented by the inverse of the
DOI: 10.1097/ CCM .0b013e31827bfc25 slope of the VR curve in the graphics attached to this article.
Obstructive Shock
Figure 3. Septic shock. Arrows indicate increase or decrease in param-
eter as appropriate. Circled N indicates normal (see text for explana- There are several pathophysiologic phenomena that cause
tion). Pms = mean systemic pressure; Rv = venous resistance. obstructive shock. Conditions such as tension pneumothorax,