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Cardiology: Open Access
Volume 5 | Issue 1 | 1 of 9
Cardio Open, 2020
e Correct Replacement for the Wrong Starling’s law is the Hydrodynamic of the
Porous Orice (G) Tube: e Complete Physics and physiological Evidence with
Clinical Relevance and Signicance
Research Article
Ahmed N Ghanem
Abstract
Introduction and objective: To report the complete evidence that Starling’s law is wrong and the correct replacement is the
hydrodynamic of the G tube. New physiological evidence is provided with clinical relevance and signicance.
Material and methods: The physics proof is based on G tube hydrodynamic. Physiological proof is based on study of the
hind limb of sheep: running plasma and later saline through the artery compared to that through the vein as regards the
formation of oedema. The clinical signicance is based on 2 studies one prospective and a 23 case series on volumetric
over load shocks (VOS).
Results: Hydrodynamic of G tube showed that proximal, akin to arterial, pressure induces suction “absorption” not “ltration”.
In Poiseuille’s tube side pressure is all positive causing ltration based on which Starling proposed his hypothesis, The
physiological evidence proves that the capillary works as G tube not Poiseuille’s tube: Oedema occurred when uids are run
through the vein but not through the artery. There was no difference using saline or plasma proteins. The wrong Starling’s
law dictates the faulty rules on uid therapy inducing VOS and causing ARDS.
Conclusion: Hydrodynamic of the G tube challenges the role attributed to arterial pressure as ltration force in Starling’s
law. A literature review shows that oncotic pressure does not work either. The new hydrodynamic of G tube is proposed to
replace Starling’s law which is wrong on both forces. The physiological proof and relevance to clinical importance on the
pathogenesis of clinical syndromes are discussed.
Mansoura University, Retired Consultant Urological Surgeon, No 1,
Jasmine Tower, President Mubarak Street, Mansoura 35511, Egypt
*Corresponding author
Ahmed N. Ghanem, Mansoura University, Retired Consultant Urological
Surgeon, No 1, Jasmine Tower, President Mubarak Street, Mansoura 35511,
Egypt
Submitted: 13 Jan 2020; Accepted: 20 Jan 2020; Published: 17 Feb 2020
Keywords: Capillary physiology; hydrodynamics; Starling’s law;
uid therapy; shock; hyponatramia; the acute respiratory distress
syndrome (ARDS); The multiple vital organ dysfunction/ failure
syndrome; (MVOD/F); Acute kidney injury (AKI)
Abbreviations
VO: Volumetric overload
VOS: Volumetric overload shocks
VOS1: Volumetric overload shock, Type 1
VOS2: Volumetric overload shock, Type2
TURS: The transurethral resection of the prostate syndrome
ARDS: The adult respiratory distress syndrome
MVOD/F: The multiple vital organ dysfunction/ failure syndrome
AKI: Acute kidney injury
HN: Hyponatraemia
BP: Arterial Blood pressure
CVP: Central venous pressure
ISF: Interstitial uid
G Tube: The Porous Orice Tube
PP: Proximal pressure to the G tube akin to arterial Blood pressure
DP: Distal Pressure to the G tube akin to venous pressure
LP: Lumen pressure of the G tube
FP: Flow pressure is the positive pressure inside the G Tube
SP: Side pressure is the negative pressure on the wall of the G Tube
Introduction
Literature review on capillary physiology and ultra-structure that
has been previously reported demonstrated that albumen’s oncotic
pressure as re-absorption force does not work in vivo; neither in
clinical practice nor in physiology. This is one of the two forces of
Starling’s law has proved wrong. My research work proves that the
other Starling’s law force of hydrostatic pressure causing ltration
is also wrong. The clinical relevance and signicance in relation to
the pathogenesis and therapy of the transurethral resection of the
ISSN: 2476-230X
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Volume 5 | Issue 1 | 2 of 9Cardio Open, 2020
prostate (TURP) syndrome, acute dilution hyponatraemia (HN),
the acute respiratory distress syndrome (ARDS) or the multiple
vital organ dysfunction/ failure (MVOD/F) syndrome and acute
kidney injury (AKI) in relation to its patho-aetiology of volumetric
overload shocks (VOS) are discussed. The key points of the complete
enlightening evidence are summarised here:-
1. Starling’s hypothesis became a law prior to the discovery of
the capillary ultra-structure and the correct physiology [1,2].
2.
The capillary has a pre-capillary sphincter as reported by Rhodin
in 1967 which makes it different from Poiseuille’s tube of
uniform diameter as my research demonstrated [3].
3.
The capillary has porous wall of intercellular slits that allow the
passage of plasma proteins as shown by Karnoveski in 1967 [4].
Hence plasma proteins cannot exert an oncotic pressure in vivo.
4. The osmotic chemical composition of various body uids is
identical to plasma proteins as demonstrated by Hendry in 1962
[5]. Plasma protein, if it works, is too weak and too slow to
effect uid absorption.
5. Guyton and Coleman (1968) demonstrated that the interstitial
uid (ISF) space has a negative pressure of -7 cm water and
Calnan et al (1972) showed that the lymph has the same negative
pressure [6,7]. The pressure under the skin is negative.
6.
The oncotic pressure of plasma proteins does not work as
absorption force neither in physiology as proved by Hendry
in 1962 nor in clinical practice demonstrated by Cochrane
Injuries Group in 1998 [5,8].
7. Inadequacy in explaining the capillary–ISF transfer in many
parts of the body as reported by Keele et al in 1982, particularly
vital organs, has previously called for reconsideration of
Starling’s hypothesis by Renkin in 1984 [9,10].
8.
My research work has demonstrated that the hydrostatic or
rather the dynamic “arterial” pressure does not cause ltration
across the wall of porous orice (G) tube as proposed by
Starling. It causes suction.
9.
This pressure induces negative side pressure gradient along
the G tube causing suction maximum near the inlet and turns
positive causing ltration maximum near the exit as based on
physics experiments on the G tube and physiological research
on the hind limb of sheep [11-13].
10.
The physiological study on the hind limb of sheep have
completed the evidence that Starling’s law is wrong as the
capillary works as G tube not Poiseulli’s tube [13].
11.
Starling’s law being wrong underlies all errors and
misconceptions on uid therapy misleading physicians into
giving too much uid during resuscitation of shock and the
acutely ill patients and during prolonged surgery thus inducing
VOS and causing ARDS or MVOD/F and AKI [14].
Here all the complete evidence based on physics and physiological
investigations that Starling’s law is wrong on both forces and
the correct replacement is the hydrodynamics of the G tube is
summarised.` Such evidence was reported as early as 1988 as
appendix in MD Thesis and 1990 in the discussion of an article
[15,16]. This physics evidence was preliminary reported in 2001 and
concluded in 2017 [11,12]. The physiological evidence was reported
in in 2017 [13]. The complete evidence with the clinical relevance
and signicance of discovering volumetric overload shocks (VOS)
inducing ARDS or MVOD/F and AKI is nalised here and now in
2020 [17-21].
Materials and Methods
The complete physics and physiological evidence and the clinical
relevance and signicance are based on:
1. Analytical literature review of articles on the capillary ultra-
structure and physiology.
2. Physics study on the hydrodynamic of G tube. Using porous
tubes with narrow inlet and measuring the dynamic components
of lumen pressure (LP), which are the ow pressure (FP) in
lumen and side pressures (SP) exerted on its wall. The factors
that affect SP including proximal pressure (PP) akin to arterial
pressure, distal pressure (DP) akin to venous pressure and the
size of the orice of the G tube were evaluated.
3.
Physiological study on the hind limb of sheep running saline and
later albumen through the artery and comparing it when uid
is run through the vein as regards to the formation of oedema
or accumulation of uid under the skin or cling membrane.
4.
Prospective clinical study on 100 consecutive transurethral
resection of the prostate (TURP) patients among whom 10
developed the TURP syndrome randomized into treatments
comparing hypertonic sodium therapy (HST) with the
conservative treatment of using volume expansion for treating
the new shock of VOS.
5. Case series of 23 patients who suffered the TURP syndrome.
The rst 3 patients were wrongly diagnosed being mistaken for a
known shock and treated with volume expansion causing ARDS
and death. The remaining 20 patients were correctly diagnosed
as VOS and treated with HST of 5%NaCl or 8.4%NaCo3 were
saved from certain death.
6.
Critical comprehensive literature review of the literature on the
TURP syndrome, HN, ARDS and uid therapy in hospitals.
Results
The results of physics experiments demonstrate that the hydrostatic
or rather the dynamic pressure in a porous orice (G) tube induced by
the high positive proximal pressure, akin to arterial pressure, induces a
negative side pressure gradient on the tube’s wall. This SP is negative
maximum at orice (Figure 1) and turns positive at the distal part
maximum near the exit (Figure 2). This produces the phenomenon
of the G tube; uid ows out from side holes near the outlet or the
‘venous’ end while it ows in by suction through holes near the inlet
or ‘arterial’ end, re-entering back into the lumen of the G tube. Fluid
around the G tube in chamber C moves in an opposite direction to
ow inside its lumen in a magnetic eld-like pattern (Figure 3).
Figure 1: Perpendicular needles inserted into a rubber orice tube
at 10, 20 and 30 mm distance from the orice, with bevels facing
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Volume 5 | Issue 1 | 3 of 9Cardio Open, 2020
downstream, demonstrate the negative energy SP gradient along
the proximal part of the tube by the sucked columns of uids in
manometer tubes from a jar 300 mm below the tube. (Reproduced
with permission of the author from BHC open access journal;
reference 12)
Figure 2: Fluid ows out autonomously through distally situated side
holes of a porous orice (G) tube where SP is positive. Air suction
occurs through side holes of the proximal part, as shown in Figure
1, but is not seen here. The uid around the G tube has magnetic
eld shape shown above the G tube. (Reproduced with permission
of the author from BHC open access journal; reference 12)
Figure 3: Shows diagram of the porous orice (G) tube enclosed in
chamber (C) based on several photographs, some of it are shown here,
demonstrating the magnetic eld-like G-C circulation phenomenon.
The proximal inow (arterial) pressure (1) pushes uid through the
orice (2) creating uid jet in the lumen of the G tube. The uid
jet creates negative side pressure gradient causing suction maximal
over the proximal half of the G tube near the inlet (3) that sucks
uid into lumen. The side pressure gradient turns positive pushing
uid out of lumen over the distal half maximally near the outlet (4).
Thus the uid around G tube inside C moves in magnetic eld-like
uid circulation (5) taking an opposite direction to lumen ow of
G tube. The inow (arterial) pressure (1) and orice (2) induce the
negative side pressure energy creating the dynamic G-C circulation
phenomenon that is rapid, autonomous and efcient in moving uid
out from the G tube lumen at (4), irrigating C at (5), then sucking it
back again at (3), maintaining net negative energy pressure (7) inside
C. The distal outow (venous) pressure (6) enhances outow at (4)
and its elevation may turn the negative energy pressure (7) inside
C into positive, increasing volume and pressure inside C chamber.
(Reproduced with permission of the author from BHC open access
journal; reference 12)
This G-C circulation phenomenon also induces a net negative
pressure in chamber (CP), surrounding the G tube, demonstrated
in (Figures 4 and 5). A negative pressure also occurs inside chamber
C, akin to that of the ISF space, causing uid to move in an opposite
direction to the main ow in the G tube lumen.
Figure 4: The net negative pressure of a closed chamber (CP)
surrounding the G tube, is demonstrated by the sucked uid in two
vertical manometer tubes from a jar 300 mm below. (Reproduced
with permission of the author from BHC open access journal;
reference 12)
Figure 5: The negative CP (Figure 4) collapses a membrane around
the G tube. This means that the G tube irrigates C chamber well
under negative pressure without accumulation of uid. In the case
of capillaries shown on the physiological investigation on the hind
limb of sheep (see text) arterial ow irrigates ISF space and cells well
under negative pressure without odema formation. While venous
ow induces oedema irrespective whether saline or plasma proteins
were used. (Reproduced with permission of the author from BHC
open access journal; reference 12)
The physiological study on the hind limb of sheep running saline and
comparing it to albumen rst through the artery and later through
vein as regards the formation of oedema or accumulation of uid
under cling membrane that replaced the skin. Oedema occurred only
when uid is run through the vein and not through the artery. This
means that the capillary works as the G tube not Poiseuille’s tube.
The G tube phenomenon irrigates ISF space and cells well without
oedema formation. There was no difference on running plasma from
running saline as circulatory uid; both uids induced oedema when
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Volume 5 | Issue 1 | 4 of 9Cardio Open, 2020
run through the vein but not when run through the artery.
The prospective study demonstrated that volumetric overload (VO)
is the most signicant factor in inducing the vascular shock of TURP
syndrome (Figure 6 and Table 1). This shock is recognized as VOS.
The correct lifesaving treatment for VOS1 of the TURP syndrome
is hypertonic sodium therapy (HST) of 5%NaCl or 8.4%NaCo3.
Figure 6: Shows the means and standard deviations of volumetric
overload in 10 symptomatic patients presenting with shock and
hyponatraemia among 100 consecutive patients during a prospective
study on transurethral resection of the prostate. The uids were of
Glycine absorbed (Gly abs), intravenously infused 5% Dextrose
(IVI Dext) Total IVI uids, Total Sodium-free uid gained (Na Free
Gain) and total uid gain in litres. (Reproduced with permission of
the author and Editor of BJU Int.; reference 16)
The case series of 23 patients demonstrated that mistaking VOS for
one of the recognized shocks such as septic or haemorrhagic shock
and treating it with further volume expansion caused ARDS and
death of the rst 3 patients. Diagnosing VOS correctly and treating
it with prompt HST saved the lives of 20 patients. The volumetric
overload in these 23 cases is shown in (Figure 7).
Figure 7: Shows volumetric overload (VO) quantity (in litres and
as percent of body weight) and types of uids. Group 1 was the 3
patients who died in the case series as they were misdiagnosed as
one of the previously known shocks and treated with further volume
expansion. Group 2 were 10 patients from the series who were
correctly diagnosed as volumetric overload shock and treated with
hypertonic sodium therapy (HST). Group 3 were 10 patients who
were seen in the prospective study and subdivided into 2 groups;
Group 3.1 of 5 patients treated with HST and Group 3.2 of 5 patients
who were treated with guarded volume expansion using isotonic
saline. (Reproduced with permission of the author from BHC open
access journal; reference 18)
VOS is of two types depending on the type of uid inducing it.
Sodium-free uid such as 1.5% Glycine and 5% Glucose induce
VOS1. The TURP syndrome and dilution hyponatraemia (HN)
represent VOS1. Sodium-based uid such as Normal Saline,
Hartmann’ solution, plasma, plasma substitute and/or blood induce
VOS2. Both VOS are always mistaken for one of the recognized
shocks and wrongly treated with volume expansion using isotonic
sodium-based uids causing ARDS and death. Discovery of VOS
has resolved the puzzles of TURP syndrome, HN and ARDS or
MVOD/F syndrome, discovering its exact patho-aetiology and
successful lifesaving therapy.
Discussion
The presented results demonstrate that the hydrodynamics of the
G tube are different from that of Hagen (1839)–Poiseuille’s tube
(1840), which in turn challenge the role attributed to arterial pressure
as the ltration force in the capillary circulation as proposed by
Starling [1]. Inow PP induces a uid jet with LP inside both the
G tube and Poiseuille’s tubes, which has the dynamic FP and SP
components. Over the proximal part of the G tube, the net effect
of the negative SP gradient is suction (Figure 1) and turns positive
causing ltration near the exit but in Poiseuille’s tube it is ltration
all along the entire length of the tube. Both the dynamic FP and SP
components of a uid jet are extensions of the well known Bernoulli
(1738) and Venturi effects.
The major difference between Poiseuille’s tube and G tube, is that
the rst induces an all positive pressure gradient which can only
cause ltration along the entire length of a tube – hence it requires
another force for re-absorption. The G tube has both its negative
and positive dynamic pressure components which autonomously
induce both absorption (Figure 1) and ltration (Figure 2) through
the G–C circulation phenomenon (Figure 3) and the net negative
CP in a surrounding uid chamber C (Figures 4 and 5). Physics of
the G–C phenomenon [11,12], with physiological evidence [13] and
clinical relevance and signicance inducing volumetric overload
shocks (VOS) [14-19] and causing ARDS or MVOD/F syndrome
and AKI [20,21] are discussed Vide Infra.
Dr Starling proposed his hypothesis >80 years prior to the discovery
of the capillary ultrastructure and correct physiology which are as
follows. He based his hypothesis on Poiseuille’s work in which the
hydrostatic pressure is a positive function of the arterial pressure
causing ltration, but in the G tube hydrodynamic as a porous orice
tube this pressure is different causing suction. Thus Starling’s low
is wrong on both forces because
1.
The capillary has a pre-capillary sphincter as reported by Rhodin
in 1967 which makes it different from Poiseuille’s tube of
uniform diameter as my research demonstrated [3].
2.
The capillary has porous wall of intercellular slits that allow the
passage of plasma proteins as shown by Karnoveski in 1967 [4].
Hence plasma proteins cannot exert an oncotic pressure in vivo.
3. The osmotic chemical composition of various body uids is
identical to plasma proteins as demonstrated by Hendry in
1962, Hence oncotic pressure if it exists is too week and too
slow force to cause absorption [5].
4.
The oncotic pressure of plasma proteins does not work as
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absorption force neither in physiology as proved by Hendry
in 1962 nor in clinical practice demonstrated by Cochrane
Injuries Group in 1998 [5,10].
5. Guyton and Coleman (1968) demonstrated that the interstitial
uid (ISF) space has a negative pressure of -7 cm water and
Calnan et al (1972) showed that the lymph has the same negative
pressure [6,7]. The pressure under the skin is negative. That
cannot be explained by Starling’s law.
6. Inadequacy in explaining the capillary–ISF transfer in many
parts of the body as reported by Keele et al in 1982, particularly
vital organs, has previously called for reconsideration of
Starling’s hypothesis by Renkin in 1984 [8,9].
7.
My research work reported here demonstrates that the
hydrostatic or rather dynamic “arterial” pressure does not cause
ltration across the wall of porous orice (G) tube as proposed
by Starling. It causes suction.
8.
This pressure induces negative side pressure gradient along
the G tube causing suction maximum near the inlet and turns
positive maximum near the exit causing ltration as based on
physics experiments and physiological research [11-13]. Venous
pressure enhances ltration and causes oedema but arterial
pressure does not- it causes absorption by suction.
9.
The physiological study on the hind limb of sheep has completed
the evidence that Starling’s law is wrong as the capillary works
as G tube not Poiseulli’s tube [13].
10.
Starling’s law being wrong underlies all errors and
misconceptions on uid therapy misleading physicians into
giving too much uid during resuscitation of shock and the
acutely ill patients and during prolonged surgery which induce
VOS causing ARDS [14-19].
11.
Received thinking that elevating central venous pre3ssure (CVP)
is synonymous with elevating arterial pressure is prevailing in
current clinical practice during uid therapy for shock and the
management of the acutely ill patients. This may be correct
during restoration therapy for hypovolemic and haemorrhagic
shock, but vascular expansion or volumetric overload (VO)
is a different issue as it induces VOS and ARDS or MVOD/F
syndrome and AKI [14-21].
12. Persistent attempts to elevate CVP up to levels of 18 to 22 cm
water are common received practice, but wrong because the
normal CVP is 0 and most textbooks report a range of –7 to
+7 cm water [9,22].
13. Clinical observations demonstrate that, in addition to the well
known effect of high venous pressure causing oedema, arterial
hypertension has no such effect, if not the exact opposite. In
clinical practice, although arterial hypertension is common, ISF
oedema is unknown among its complications.
14.
In the G–C model, a minor increase in DP increases uid volume
in chamber C reverting CP from negative to positive while
slowing the G–C circulation [11,12]. Increasing DP has similar
effect to decreasing PP on the G–C circulation and chamber
pressure and volume.
15.
Vascular expansion causes VO shocks [14-19]. There is no
doubt that the erroneous Starling’s law is responsible for the
many errors and misconceptions prevailing on uid therapy
for shock and the acutely ill patients which mislead physicians
into giving too much uid that induce VOS causing MVOD/F
syndrome or (ARDS and AKI [14-21].
The physiological proof that the capillary works as G tube
A physiological study was conducted on the hind limb of sheep
brought from the Butcher shop and wrapped in a cling lm to
replace the skin. Both normal saline and plasma proteins were
used as circulatory uid, and compared [13]. An electric pump was
used to circulate uid once through the main artery and compared
it to another running uid through the main vein. The formation
of oedema was observed by the increase in the limp weight and
accumulation of uid under the cling lm that replaced the skin.
Here is the abstract of this physiological study.
Objective
To report physiological evidence that the capillary works as a porous
orice (G) tube proving that Starling’s law is wrong.
Material and Methods
The G tube has a negative side pressure (SP) exerted on its wall.
The G tube is akin to capillary and when enclosed in a chamber (C),
akin to interstitial uid space, demonstrating the G-C circulation
phenomenon (Figure 3).
Here we report the results of experiments on the hind limb of sheep;
rst when the uid is passed through the artery and later when
passed through the vein. We monitored the occurrence of oedema
of the limb comparing the two circulations. We used normal saline
and compared it to plasma proteins in different set of experiments.
Results
The inow pressure induces negative SP in the G tube which is
responsible for absorption and G-C phenomenon: an autonomous
magnetic eld-like G–C circulation occurs between uid in the G
tube’s lumen and a surrounding uid compartment C. The hind limb
acted as normal without oedema and has a negative interstitial (ISF)
pressure when the uid is passed through the artery i.e. acting like
the G tube. There was gross oedema with increase in weight of the
limb when the uid was passed through the vein when the capillary
acts like Poiseuille tube. There was no difference between using
saline or plasma proteins.
Conclusion
The reported studies afrm that the capillary works as G tube
effecting circulation with ISF which causes negative ISF pressure.
When the circulation is reversed through the vein it acted like
Poiseuille’s tube causing gross oedema and positive ISF pressure.
This is the physiological proof that Starling’s law is wrong.”
The clinical relevance and signicance of correcting Starling’s law
Over 32 years of my career life I did many studies, some reported as
communications, MD Thesis and articles [15-21, 23-29]. A summary
of some overlooked issues, new concepts and discoveries made since
my initial brain storming thoughts were reported at The BMJ and
The Lancet is mentioned here [23-25]. The shock that complicates
overzealous fluid therapy during poly-trauma resuscitation,
recognized as VOS2, may complicate various recognized shocks,
diverse diseases requiring uid therapy or parentral nutrition on
intensive care units and during prolonged major surgery [30-42]. The
prevalence of morbidity and mortality of this condition known as
ARDS is staggering yet if it has attracted a fraction of the attention
given to AIDS, it should have been resolved by now [40].
There is no doubt that correcting the faulty Starling’s law has led to
the discovery of volumetric overload shocks (VOS) that complicate
iatrogenic overzealous uid infusion inducing diverse clinical
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presentations depending on the type of uid gained, volume and
time [14-19]. The severity of the signs is directly proportional to the
VO but inversely to time (VO/T). Fluid type determines the changes
of serum solutes and presentation; sodium-free uids (VO1) inducing
VOS1 are characterized with hyponatraemia (HN) with a primary
nadir proportional to severity occurring during or immediately after
surgery as dilution of the extracellular uid [15,16].
The gain of VO1 such as 5% Dextruse, and 1.5% Glycine may occur
either via excessive infusion or inadvertent absorption of irrigating
uids used in endoscopic surgery- known as TURP syndrome or
hyponatraemic shock [15, 16, 31, 35, 36,38,39]. This shock was
even rst reported as experimentally induced in in dogs [32]. It also
affects women undergoing trans-cervical endometrial resection and
other endoscopic surgery [37]. Other patients including women and
children infused with excessive VO1 uids such as 5% dextrose
were reported [38,39]. These are examples of VOS type 1 (VOS1).
Correcting Starling’s law has not only identied the exact patho-
aetiology of the TURP syndrome and acute hyponatraemia (HN)
but also has rejuvenated a highly successful lifesaving therapy
for it; namely; hypertonic sodium therapy (HST) of 5%NaCl or
8.4%NaCo3.
This VOS1 is characterized by the marker of HN presents with
cardiovascular shock. It may present with cardiac arrest or respiratory
arrest in isolation or a combination of both “cardiopulmonary
arrest” to anaesthetists and surgeons in theatre and with coma to
physicians later [14-19,30-33,37-39]. Manifestations of respiratory,
cardiac, renal and hepatic dysfunction or failures are also evident
and are recognized as MVOD/F syndrome which is the new name
for ARDS [20,21,41]. Acute kidney injury (AKI) prevents urinary
excretion and sodium loss, so serum HN in VO1 shock is mainly
dilution. The hypotension of VO1 is usually mistaken for known
shocks of haemorrhage or septicaemia [17-19]. Hence, it is wrongly
treated with further vascular expansion using crystalloids, colloids
or substitutes and blood. Such VO1 shock and its hypertonic
sodium therapy (HST) of 5% NaCl was reported 7 decades ago
and rejuvenated as successful lifesaving therapy but it was thought
contra-indicated until it recently rectied by the authorities on HN
[14-18,22,23,30,31,38,39]. Recognizing VOS1 has also helped in
recognizing VOS2 that resolved the puzzle of the acute respiratory
distress syndrome (ARDS) [21].
VOS2 is induced by sodium-based uids such as crystalloids of
normal saline and Hartman’s solution, colloids such as plasma and
plasma substitutes and blood. Although better tolerated it induce
VOS2 without serological markers, afrming the concept of VOS
but it remains disbelieved. A normal daily intake of 3.5 litres (L)
of uid causes signs when intravenously infused over 2–3 h but
can be a serious gain in <1 h. Why is it so difcult to recognize
these facts on encountering serious cases even of VOS1 that is
characterized with HN? Although the systemic and bizarre signs
of severe TURP syndrome are well documented in case reports,
it is extremely difcult to relate to VO/T and uid type, even on
monitoring the gained volume, measuring and replacing blood loss
and excluding septicaemia.
The complex signs of cardiovascular disturbance of shock and
MVOD/F of the TURP syndrome are very variable in severity,
up to cardiac or cardiopulmonary arrest and death, with many
presentation masks and differential diagnoses. Hence, when seen
in the complex surgical setting, they are wrongly attributed to known
causes of shock, coma, respiratory distress, renal and heart failure
or arrest as signs of MVOD/F that may occur in any combinations.
Of the well documented presentation masks of VOS1, one is shock
apparent to anaesthetists and surgeons during or immediately after
the surgery and another is coma recognised later by physicians. More
important, neither the concept nor mechanism of VOS by disturbing
capillary dynamics has been recognized, despite explaining the
patho-aetiology of the TURP syndrome and shock, highlighting its
link with MVOD/F syndrome or APRDS [14-20,21,36-38,40]. A
prospective study on 100 TURP patients among whom 10 suffered
the TURP syndrome demonstrated that VO is the most signicant
factor in its patho-etiology (Figure 6 and Table 1) [16,17]. Also a
case series of 23 patients afrmed VO as the correct patho-aetiology
of the TURP syndrome (Figure 7) [18].
Table 1: shows the multiple regression analysis of total per-operative
uid gain, drop in measured serum osmolality (OsmM), sodium,
albumin, Hb and increase in serum glycine occurring immediately
post-operatively in relation to signs of the TURP syndrome.
Volumetric gain and hypo-osmolality are the only signicant
factors. Volumetric gain is most highly signicant. (Reproduced
with permission of the author and Editor of BJU Int.; reference 16)
Parameter Value Std. Err Std. Value T Value P
Intercept 0.773
Fluid Gain (l) 0.847 0.228 1.044 3.721 0.0001
Osmolality 0.033 00.014 -0.375 2.42 0.0212
Na+ (C_B) 0.095 0.049 0.616 1.95 0.0597
Alb (C_B) 0.062 0.087 0.239 0.713 0.4809
Hb (C_B) -0.282 0.246 -0.368 1.149 0.2587
Glycine (C_B) -4.973E-5 5.975E-5 -0.242 0.832 0.4112
There is no doubt that the erroneous Starling’s law is responsible
for the induction of the two newly discovered VOS. Volumetric
overload shocks (VOS) are iatrogenic complications of uid
therapy in hospitals [17-19]. It is common but overlooked and
underestimated. When it is realized that acute dilution hyponatraemia
(HN) and ARDS is representative of each type of the two VOS it
would be appreciated that it has staggering morbidity, cost and
mortality. It affects hundreds of thousands of patients worldwide
each year including surgical, urological and obstetric patients of
men, women and children undergoing surgery. It concerns new
discoveries in medicine and physiology [43]. This article brings
these new discoveries into the attention of readers, particularly
surgeons and anaesthetists as these condition concerns them most.
Other scientic discoveries in addition to the 2 VOS are proving
the physiological law of Starling for the capillary-interstitial uid
transfer wrong and nding a new correct replacement which is the
hydrodynamic of the porous orice (G) tube (Figure 3) as presented
here. Starling’s law being wrong has resulted in many errors and
misconceptions on uid therapy during prolonged surgery and the
resuscitation of shock and the acutely ill patients. This misleads
physicians into giving too much uid which induces VOS, causing
cardiac arrest or respiratory arrest or both “cardiopulmonary arrest”
immediately in theatre or ARDS later [20,21,37,44,45,49,50].
VOS are two types depending on the type of uid: VOS1 is induced
by sodium-free uid such as 5% Glucose and/or 1.5% Glycine used
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as irrigating uid during the transurethral resection of the prostate
(TURP) surgery. It is known in urology as the TURP syndrome or
hyponatraemic shock [16,31,36].
This VOS1 is induced by 1.5% Glycine absorption and 5%
glucose infusion of about 3.5-5 liters or >5% of body weight
and is characterized with dilution hyponatraemia (HN) [46-48].
Hyponatraemia has 2 nadirs and 2 paradoxes making it dynamic
and illusive [46,47]. The 2 nadirs are: The immediate drop of
serum sodium level as result of dilution of the extra-cellular uid
that occurs during or immediately after surgery. The second nadir
is that occurring later within 24 hours after water shift into the
intracellular compartment causing spontaneous elevation of serum
sodium level towards normal, yet the clinical picture gets worse
due to generalized cellular oedema. This cellular oedema manifests
as MVOD/F syndrome, ARDS or AKI. The 2 paradoxes are: A
pathological volumetric overload induces hypotensive shock of
VOS and acute renal failure (ARF) or AKI which is paradoxical
to the response of physiological volume replacement that treats
hypotensive shock and induces diuresis.
VOS1 currently has a lifesaving therapy of hypertonic sodium
therapy (HST) of 5% NaCl or 8.4% Co3 [48]. It may present with
cardiopulmonary arrest or one or more of the other manifestations
of MVOD/F syndrome- being the new name for ARDS [40,41,44].
The clinical manifestations include in addition to cardiorespiratory
features: coma with convulsions and paralysis, AKI and hepatic
dysfunction. It also causes coagulopathies and excessive bleeding
at the surgical site [34]. VOS1 affects women too during the trans-
cervical resection of endometrium due to 1.5% Glycine absorption,
and during Caesarean section due to excessive 5% Glucose infusion
[37,38,39,44].
VOS is always mistaken for one of the recognized shocks such as
haemorrhagic and septic shocks hence wrongly treated with further
volume expansion using sodium-based isotonic uids. This induces
VOS2 and cardiopulmonary arrest that has no serum markers of
HN and causes ARDS in patients who survive a little longer [45].
Multiple regression analysis has proved that volumetric overload
is the most signicant factor in causing the clinical picture of VOS
(Figures 6 and 7 and Table 1) [16]. Cardiac arrest or respiratory
arrest in isolation, or a combination of both have been reported as
immediate presentation of the TURP syndrome induced by 1.5%
Glycine and dilution hyponatraemia induced by 5% Glucose during
surgery as representative of VOS1 [37,38,39,44,49,50].
Volumetric overload shock type 2 (VOS2) is induced by massive
infusion of sodium-based uids such as normal saline, Hartmann,
plasma, plasma substitutes and/or blood. VOS2 may complicate
VOS1 or is induced by sodium-based uid during uid therapy for
resuscitation of shock and the critically ill and prolonged surgery and
presents with ARDS later [14-21,40]. Volumetric gain of 12-14 litres
of sodium-based uids reported in the rst article on ARDS which
is the only article in the whole literature, other than the articles of
mine referenced here, that documents the volume of retained uid
in ARDS [40]. The question of: “Does Raising the Central Venous
Pressure (CVP) in Treating Shock with Fluids Induce Volumetric
Overload Shocks (VOS)?” has been positively answered [51,52].
The above mentioned discoveries should make the Medical World
wake up, pay attention and listen to what this article has to say [53].
Summary
Hydrodynamic studies on a porous orice (G) tube, based on
capillary ultra-structure, demonstrate results which differ from
Poiseuille’s in a strait uniform tube and hence challenge the role
attributed to arterial pressure as a ltration force in Starling’s law. A
perspective literature review shows that the oncotic pressure force
has been previously cancelled and the law has failed to explain the
capillary–ISF transfer in most parts of the body.
A concept based on a new hydrodynamic phenomenon is proposed
for the capillary–ISF circulation. It explains this vital circulation in
every organ and tissue under both physiological and pathological
conditions. A rapid autonomous dynamic magnetic eld-like
G–C circulation occurs between uid in the G tube’s lumen and a
surrounding uid compartment C. Based on results of studies on a
circulatory model incorporating the G–C apparatus, factors which
initiate, regulate and affect the G–C circulation, its physiological
and haemodynamic relevance and its clinical importance to the
pathogenesis of oedema, shock and MVOD/F syndrome or ARDS
and AKI are given.
The presented evidence does not only prove that Starling’s law is
wrong, but also provide the correct replacement; the hydrodynamic
of the G tube explaining the capillary-ISF circulation in every organ
and tissue of the bogy. Also the physiological evidence on capillary
working as G tube not Poiseuille’s tube is provided. The presented
evidence proves without a doubt that Starling’s law is wrong and
provide its correct replacement of the G tube hydrodynamic. This
erroneous law is responsible for the many errors and misconception
prevailing in uid therapy during resuscitation of shock and acutely
ill patients misleading physicians into giving too much uid and
inducing VOS causing MVOD/F or ARDS and AKI.
VOS are common iatrogenic complication of uid therapy in
hospitals that is overlooked and underestimated. It may present in
theatre as cardiopulmonary arrest or later with coma and ARDS.
VOS is 2 types; VOS1 and VOS2. VOS1 is induced by3.5-5 litres
of sodium-free uid and is characterized with dilution HN that
has 2 nadirs and 2 paradoxes, is most dynamic and illusive and
currently has a lifesaving therapy of HST. VOS2 may complicate
VOS1 or occur de novo complicating sodium based uid therapy
during resuscitation of shock, acutely ill patients and prolonged
surgery. It has no obvious serological markers or none. Many errors
and misconceptions mislead physicians into giving too much uid
for resuscitation due to faulty rules on uid therapy dictated by
the wrong Starling’s law. The correct replacement for this law is
the hydrodynamic of the porous orice (G) tube. These scientic
discoveries should make the Medical World wake up, pay attention
and listen to what this article has to say.
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