The Effect of

Mechanical Ventilation on
Hepatosplanchnic Perfusion

Trisna Haryo Prasetyo

JCCA Symposium 2022
 • Sirkulasi splanknik dan signifikansinya (volume)
• Pasien critical care: perubahan yang terjadi +
perubahan apa pada splanknik
• Why we concern about splanchnic perfusion?
• Ventilator mekanik: apa yang terjadi.
OUTLINE • Faktor MV apa saja yang paling mempengaruhi
sirkulasi splanknik: TV, PEEP, PIP?
• GI complications associated with MV
• Obat2an: mana saja dan apa pengaruhnya ke
splanknik
• Hepatic perfusion
Hepatosplanchnic
Circulation Splanchnic circulation is a complex system:
Blood flow to the gastrointestinal organs including stomach,
liver, spleen, pancreas, small intestine and large intestine.

Important functions depend on its normal

operation:
Digestion and Maintenance of Successful healing
absorption within the mucosal of surgical
the gut, barrier and anastomoses
Hepatosplanchnic
Circulation
3 major branches
• Coeliac artery
• Superior mesenteric
artery
• Inferior mesenteric
artery

+
Portal Vein : circulation
delivers the majority of the
blood flow to the liver

BJA Educ, Volume 16, Issue 2, February 2016, Pages 66–71

Coeliac Artery Superior Mesenteric Inferior Mesenteric
Artery (SMA) Artery
Hepatosplanchnic 500
Circulation
ml/menit

3 major branches 700

ml/menit
• Coeliac artery
• Superior mesenteric
artery 700
ml/menit
• Inferior mesenteric
artery

+
Portal Vein : circulation
delivers the majority of the
blood flow to the liver 400
ml/menit

BJA Educ, Volume 16, Issue 2, February 2016, Pages 66–71

 • Splanchnic circulation: highly adaptive

• Splanchnic Blood Flow

Physiology • Resting : 30 ml/min/100 g of tissue (25-30% CO)
of Splanchnic • <10 ml/min/100 g in low Cardiac Output
• 250 ml/min/100 g after a Meal
Blood Flow
• The mechanism:
• intrinsic (local metabolic vs myogenic)
• extrinsic (autonomic nervous system)
• humoral (local or circulating vasoactive substances)

BJA Educ, Volume 16, Issue 2, February 2016, Pages 66–71

Intrinsic Control

• AUTOREGULATORY CAPCITY → MAINTAIN CONSTAN BLOOD FLOW (BF)

• MECHANISM :

1. METABOLIC :
Balance between oxygen supply & demand
✓ Accumulation H+, K+, adenosin or CO2 produce vasodilation → restore BF
✓ Increase O2 delivery → induce vasoconstriction.

2. MYOGENIC
Vessels respond to an increase in transmural pressure or stretch by constricting →
restore BF to baseline levels.
Mediated through opening cation channels (Na+) → Depolarization → Activates Ca2+
channel → elevating intracell Ca2+ concentration → smooth muscle contraction
EXTRINSIC CONTROL
Sympathetic innervation
Noradrenalin mediating a-adrenergic
vasoconstriction.
Sympathetic vasoconstriction:
• physiological (exercise)
• pathological (major hemorrhage)
Parasympathetic innervations (From
vagal & pelvic nerves synapse)
Activation of M1 receptor by
acetylcholine in the endothelial layer →
NO ↑ → vascular smooth muscle
relaxation → BF ↑
Sympathetic stimulation
redistribute blood flow to muscular layer of vascular wall
by decreasing mucosal perfusion → mucosal ischemia
Humoral Control
• Circulating vasoactive mediators (Exogenous or Endogenous):

• Increase Mucosal metabolic activity → adenosin & CO2 → BF ↑

• Hiperosmolar condition exerted by the absorption of nutrients → BF ↑

• Hiperosmolar intraluminal → Intracellular Na+ ↑ → activation Na+/Ca2+

exchanger → intracellular Ca2+↑ → activation NO synthase → NO ↑

• Peptide hormones (cholecystokinin, secretin & gastrin) released locally during

digestion → BF ↑
Vasoactive mediators
of the splanchnic
circulation

• BJA Education, Vol 16, Number 2, 2016

Why we concern Hepato- Splanchnic Perfusion?
LOW SYSTEMIC BLOOD FLOW:
HEMORHAGE

VITAL PERFUSION IS MAINTAINED

At the EXPENSE of
PERFUSION OF VISCERAL ORGAN

ISCHAEMIA → TISSUE DAMAGE → NECROSIS

TRANSLOCATION BACTERIAL & ENDOTOXIN

No drug available that selectively

improves splanchnic perfusion
Splanchnic Perfusion in
Low-Flow states &
mechanism of
impairment.
• Vasoconstrictive response to
circulatory shock is mediated
by
• symphatetic nervous
system,
• renin-angiotensin system
• vasopressin.
• When a-adrenergic
receptors stimulated →
autotransfusion → improve
heart performance.
 Danger • Low blood flow to the gut with and without reperfusion is
associated with:
associated • increased permeability of the gut wall,
• endotoxaemia,
inadequate • presence of bacteria in abdominal lymph nodes &
splanchnic thoracic duct
• possibly bacteraemia.
blood flow • Low gastric mucosal pH associated with increase morbidity
& mortality.
• Sepsis trial : Liver disfunction associated with a markedly
higher mortality rate.
• Ability to increase splanchnic oxygen delivery → lower
mortality rate.
 Compromised cardiac function

When is Surgical procedure in critically ill

splanchnic
at risk for
inadequate Extracorporeal Organ Support
perfusion?
Abdominal compartment
syndrome
 MECHANICAL
VENTILATION:
WHAT HAPPENS?
 Compromised cardiac function

When is Surgical procedure in critically ill

splanchnic
at risk for
inadequate Extracorporeal Organ Support
perfusion?
Abdominal compartment
syndrome
Cardiovascular Effects of
Positive Pressure Ventilation
Which components are
of concern? TIDAL VOLUME

PEEP

INSPIRATORY PRESSURE

Mode of Ventilation
 • IPPV → Preload Reduction → Cardiac Output ↓ →
SPLANCHNIC PERFUSION↓

Intermitent Very large VT

Positive High PEEP
High Inspiratory Pressure
Pressure
Ventilation
hepatic venous pressures ↑
(IPPV) mesenteric vascular resistance
portal blood flow ↓
 Increase Cytokine Release by
High Tidal Volume Mechanical Ventilation

Induce Cytokine Release:

High VT
modify inflammatory
responses irrespective of the
underlying lung injury.
SPLANCHNIC
TNF alpha & IL 8
HYPOPERFUSION
&
translocation of cytokines
INTESTINAL SMOOTH
lungs ⇆ systemic MUSCLE IMPAIRMENT
circulation
 Has been shown in animal models to
be dose dependent:
• PEEP decrease venous return →
reduce preload → reduce
PEEP on Splanchnic cardiac output → SPLANCHNIC
HYPOPERFUSION.
Blood Flow • More pronounced at PEEP 15-
20 cm H2O.
• In Rats, addition of 10 cm H2O
PEEP → reduce 31% Cardiac
output & 75 % mesenteric BF.
 • PEEP also promotes plasma-renin-
angiotensin-aldosterone activity, as well
as catecholamine release, which limits
splanchnic hypoperfusion.

• High PEEP levels interfere with mesenteric

PEEP on Splanchnic leukocyte-endothelial interaction.
Blood Flow • In rats with healthy lungs, 10 mbar of PEEP
was associated with an increase in the
number of rolling, adherent, and migrated
leukocytes when compared with
mechanical ventilation with 0 or 5 mbar
PEEP.
T0 T1 T2
PEEP administration results to the impairment of splanchnic tissue perfusion
PEEP OF 10-20 CM H2O does not affect splanchnic perfusion and is hemodynamically well tolerated in most
patients with ARDS, including those receiving inotropic support

Indian J rit Care Med 2009 Vol 13

 • NORMAL VENTILATION PRESSURE : adverse effects
appear to be minimal.
• SUSTAINED RECRUITEMENT MANEUVRE: associated
with a worsening in splanchnic oxygen delivery,
despite improving arterial oxygenation.
Ventilation • SPONTANEOUS breathing efforts during APRV:
improve both cardiac output and splanchnic
and IPPV perfusion.
• PRONE VENTILATION does not affect splanchnic
perfusion, provided care is taken to avoid intra-
abdominal hypertension.
• PERMISSIVE HYPERCAPNIA helps to maintain
splanchnic perfusion.
APRV with spontaneous breathing will decrease intra thoracic pressure, and increase venous
return, and cardiac output.

Anesthesiology 2003;99:1137-44
 Intestinal Blood Flow

Maintaining spontaneous breathing with APRV was more effective in improving intestinal mucosal-
submucosal perfusion than reducing PAW and VT and concomitant with better oxygenation,
essentially improved mucosal oxygen supply throughout the intestine.
Hepatic
Complications
• Normal adult liver → dual
blood flow and oxygen supply
• 2/3 hepatic BF & ½
oxygen supply : portal
vein
• The rest : hepatic artery.
Mechanical Ventilation on Hepatic Circulation
POSITIVE PRESSURE VENTILATION SPONTANEOUS BREATHING DURING APRV

CARDIAC OUTPUT DIAPHRAGM DESCENT

REDUCTION

DIRECT COMPRESSION
GLOBAL HEPATIC OF THE LIVER
BLOOD FLOW DROP PARENCHYMA

INCREASE HEPATIC VASCULAR RESISTANCE

1. HIGHER HEPATIC VENOUS OXYGEN
SATURATION
IMPEDES PORTAL VENOUS FLOW 2. BETTER LACTATE ELIMINATION
Mechanical Ventilation on Hepatic Circulation
HIGH PEEP (15 CM H2O) DECREASE VT

PERMISSIVE HYPERCPNIA

INCREASE BLOOD FLOW

REDUCE BLOOD FLOW

1. DECREASE HEPATIC VEIN SATURATION

2. DECREASE HEPATIC GLUCOSE PRODUCTION SYMPATHETIC STIMULATION
Medication on Mechanical Ventilation

• OPIAT
• decrease gut motility
• SEDATION:
BENZODIAZEPIN • impair venous return

→alter hemodynamic parameters

• VASOPRESSOR
• INOTROPES
→ reduce mesenteric blood flow
→ stress-related mucosal disease
 GIT complications
• Interaction between PPV and the GI tract is a complex one.
• Gastrointestinal changes are reported frequently in critically
ill patients receiving PPV.
• The true incidence of GI complications is not known, but it.
Is reported to be up to 100% for those receiving PPV for
more than 3 days.
• Splanchnic hypoperfusion seems to play a pivotal role in the
pathogenesis of these complications, including mucosal
damage, motility disorders & mesenteric ischemia.
Stress-Related Mucosal Disease (SRMD)

• Most common cause of GI bleeding in patients receiving mechanical

ventilation.
• 74-100% → endoscopically detectable lesions in the gastric mucosa within
hours after admission.
• These lesions are most frequently in the acid-producing areas of the
stomach, in contrast to peptic ulcers (common in the antrum and the
duodenal bulbs).
• Overt stress-related GI bleeding occurs in up to 5% of critically ill patients.
MEKANISME SRMD
(Stress Related
Mucosal Damage)
 • Inadequate splanchnic perfusion in critically
ill patients ~ increased morbidity and
mortality
• Splanchnic blood flow may become
insufficient as a result of treatment
modalities: MV, medications
Conclusion • The maintenance of cardiac output during
mechanical ventilation should prevent
potential impairment of splanchnic
perfusion.
• Ventilation Mode, Tidal Volume, PEEP and
Peak Inspiration Pressure are factors that
can maintain cardiac output.