Management of Non Cardiogenic

Shock
A Perspective of Septic Shock

Philia Setiawan, MD
 Shock Classification

Hypovolemic : hemorrhagic, non hemorrhagic

Cardiogenic : myocardial, arrythmias
Distributive : Septic, anaphylactic,
neurogenic
Obstructive : tamponade, pneumothorax,
pulmonary embolism
 CARDIOGENIC
SHOCK

DISTRIBUTIVE SEPTIC OBSTRUCTIV

SHOCK SHOCK E SHOCK

HYPOVOLEMIC
 Shock Definition

SHOCK is defined as
a syndrome of impairment of tissue
perfusion and oxygenation
 Sepsis, Severe Sepsis, Sepsis induced
hypotension and Septic Shock
(SSC 2012)
Sepsis is defined as the presence (probable or
documented) of infection together with its
manifestation.
Severe sepsis is sepsis with sepsis induced organ
dysfunction and hypoperfusion
Sepsis induced hypotension is defined as SBP <90,
MAP<70 or SBP decrease > 40
Septic shock is defined as sepsis-induced hypotension persisting
despite adequate fluid resuscitation.
Sepsis-induced tissue hypoperfusion is defined as infection-
induced hypotension, elevated lactate, or oliguria.
 Pathophysiology of Septic shock

Myocardial
depression

Vasodilata Maldistri
tion bution
Septic
Shock

3 major cardiovascular insult in sepsis are : maldistribution of blood flow ,

vasodilation and myocardial depression
 Other new issues

Mitochondrial dysfunction : ROS formation,

Respiratory Complex dearrangement

Enzymatic degradation of endothelial

glycocalyx induces vascular leakage
 Vasodilatation
Cytokines + other metabolites (prostaglandins)
Intracellular hypoxia

Endothelial derived Nitric Oxide

Lactate increased/H+

Activation of K-ATP channel Changes in cell-wall transport mechanism

Ca2+ influx

Cellualar Ca2+

Vasodilatation and
Resistance to vasopressor agent
Maldistribution of Blood Flow

Various inflammatory mediators

1. Not all vessels are dilated, some

arterioles remain vasoconstriction
2. PLUG formation
3. Shunt in tissue perfusion
Myocardial Depression

Endotoxins TLR4

C5 Cytokines NO

Impaired Ca2+ uptake, release and

decreased calcium channel
sensitivity

Myocyte dysfunction
 Clinical view of Myocardial depression in Sepsis

Decreased LVEF < 50

Increased of Trop I and T correlate with the duration of

hypotension and the intensity of vasopressor and associated
with degree of LV dysfunction (Ver Elst K M, 2000)

Increase BNP levels (>230 pg/ml) associated with reduced LV

function (Rivers, 2007)

Ventricular enlargement during fluid resuscitation is to

maintain cardiac output. Those patients presenting with
ventricular relaxation impairment or a drop in EF exhibited
the worst prognosis (Bouhemad, 2009)
 Hemodynamic abnormality detection
Macro circulation :
- BP, HR, CVP, Urine production
- Chest XRay
- Echocardiography
- Co/CI, SVR : invasive, non invasive

Microcirculation :
- BE, Lactate, gastric tonometri (pCO2),
Sublingual pCO2
- OPS : microcirculation blood flow
- T (Core and peripheral temperature difference)
- ScvO2

Mitochondrial dysfunction
Treatment: Supportive and Causal
SSC, 2012
 Recent recommendation

Vasopressor earlier despite fluid resuscitation

to restore coronary blood flow
Alternative of Improving microcirculation :
Dobutamin, NTG, Levosimendan ?
 Nitroglycerine (NTG) restores
microcirculation ?
Can Ince, 1990s : using Orthogonal Polarized
Spectral showed the improvement of
microcirculation during septic shock

Boerma, 2010 : NTG did not show significant

difference of improving microcirculation in
stricht resuscitation protocol in septic patients
to placebo
 Levosimendan : achieving better
microcirculation ?

A Calcium sensitizer by binding to troponin c : Inotropic positive

and vasodilator
 Levosimendan Controversies :
Improving heart performance: decreases
LVEDV, PAOP and increases CI and LVEF
(Morelli, 2005)

Improving organ perfusion: increases gastric

mucosal flow, urine production (Morelli, 2005)

Antioxidant (Torraco, 2014)

Levosimendam controversies

Levosimendan for the prevention of acute organ dysfunction

Gordon AC et al, NEJM 2016

Method : Randomized Clinical Trial,

- Levosimendan decreases severity of organ dysfunction
(Sequential Organ Failure Assessment= 1-4 in 5 organs
= 20 max score) for 28 days
- Weaning from Mech-Ven
- Mortality in 28 days

Random assigned :
- 0.05-0.2 micro/kgBW/min for 24 hs
- Placebo

Adverse event
Overall Survival
Summary: Treatment for Septic Shock

Fluid Resuscitation and pharmacological

hemodynamic support
Earlier vasopressor during fluid resuscitation
Microcirculation improvement
Culture and Antibiotics
Source control
 Summary
Severe sepsis and septic shock mortality from 2002
2010 : 37% - 30% despite of SSC guidelines

Guidelines make the life of the physician easier and

quicker decision

One size does not fit all

Tailored treatment is a new recommendation