The SHOCK

Prof.dr.Şerban Bubenek MD
 Physiology of Cardiovascular System
• CO = SV x HR (Normal = 4.0 - 8.0 l/min)

• MAP = Dist. Pressure + 1/3 Pulse Pressure

(Normal = 70 - 105 mmHg)

MAP = CO x SVR

CO and Stroke Volume

1. Preload (volume)
2. After load (SVR) S.V.
3. Contractility
4. Heart Rate
 SHOCK = disequilibrium between DO2 and VO2
Oxygen delivery DO2 = CO x CaO2
CaO2 = (SaO2 x 1,36 x Hb) + (0,0031 x PaO2)

Hb = 15, SaO2 100 %, PaO2 100 mm.Hg

CaO2 = 20 ml.O2 / 100 ml

CO =5 l. / min DO2 = 5 x 20 x 10 =1000 ml O2 / min

Oxygen consumption VO2 = CO x (CaO2 - CvO2)

arterial-venous difference : ∆(a-v)O2 = CaO2 - CvO2

CvO2 = (SvO2 x 1,36 x Hb) + (0,0031 x PvO2)

CvO2 = 15 ml.O2 / 100 ml
VO2 = 5 x 5 x 10 = 250 ml.O2 / min
 again:

VO2 = DC ( CaO2-CvO2)

VO2 = DCx Hb ( SaO2 – SvO2)

SvO2 = SaO2 – VO2

DCx Hb

(TAM – PVC) = DC x RVS

CaO2 = 20 ccO2/dl CvO2 = 15 ccO2/dl
 SHOCK - 2014
Shock is best defined as a life-threatening, generalized form of
acute circulatory failure associated with inadequate oxygen utilization by the
cells.

• It is a state in which the circulation is unable to deliver sufficient oxygen to

meet the demands of the tissues, resulting in cellular dysfunction.

• The result is cellular dysoxia, i.e. the loss of the physiological independence
between oxygen delivery (DO2) and oxygen consumption (VO2), associated
with increased lactate levels !
SHOCK
 PHYSIOPATHOLOGY
Shock= severe disequilibrium between DO2 and VO2

CvO2 CaO2
DO2

CaO2

VO2
 SHOCK
1743 Henri Francois Le Dron

Physiopathology = disequilibrium DO2 – VO2

causes

DO2 VO2
• SEPTIC SHOCK
– PRecharge ( hypovolemic S. )
CO CO
– Contractility (cardiogenic S. )
(a Hyperdinamic form of shock )
–- PR, Contr + Postcharge
(obstructive shock)
all
– 3 are hypodinamic forms of shock

other forms of shock: 1. Anafilactic S.

HYPODINAMIC SHOCK

+: the SKIN !
Hyperdinamic SHOCK= VO2
VO2 DO2

Cardiac
VO2 OUTPUT

O2
VO2 demand
s
 RASPUNS LA AGRESIUNE MAJORA
1. Restabilirea stabilitatii cardio-vasculare
SCOP
2. Mentinerea aportului de O2 la nivel tisular
Raspuns: 3. Mobilizare substrat energetic
-Nespecific 4. Minimalizarea durerii
5. Vindecarea plagii
- Generalizat

AGRESIUNE = orice STRES

-pierdere LEC
-injurie tisulară arsură, trauma, chirurgie, pancreatită
-ischemie prelungită
-INFECTIE
 STIMULII PRIMARI AI
REFL. Neuroendocrine AFERENTE

a) Modif. VSCE
O2
b) Modif. conc. CO2
H+
c) Durere si emotie
d) Modif. Substratului
e) temperatura
f) Infectia
g) plaga
 RSA
EFERENTE
I. Raspuns NEURO-ENDOCRIN
• T.R. vegetativ CATECOLAMINE
Rasp glucagon, insulina
endocrin
• Axa hipot-hipof cortizol
tiroxina
STH
vasopresina
Rasp CRF
umoral hipotal hipofiza ACTH
VIP endorfine
catecol. MSR
II. RASPUNS INFLAMATOR
eliberare peptide mici local
efect la distanta
SIRS systemic inflammatory response syndrome

III. Raspuns CELULAR

 Clasificare în funcţie de tipul reacţiei
hemodinamice la şoc
 
A – reacţia hipodinamică ( şoc hipodinamic)
B – reacţia hiperdinamică (şoc hiperdinamic)
C – reacţia tip colaps
SOCUL si REACTIA HIPODINAMICA
Reacţia hipodinamică poate fi generată prin scăderea volumului sanguin circulant ca în
şocul hipovolemic (scade presarcina şi apoi debitul cardiac), sau prin scăderea primară a
debitului cardiac ca în şocul cardiogen.

Macrocirculaţie:
- activarea baroreceptorilor şi declanşarea reacţiei simpato-adrenergice (RSA) cu
eliberarea de catecolamine la nivelul terminaţiilor libere simpatice şi a
medulosuprarenalei.

în două etape:

– prima etapă cuprinde stimularea baroreceptorilor de joasă presiune din AD şi

declanşarea unei RSA cu venoconstricţie care produce creşterea întoarcerii venoase şi deci a
presarcinii şi menţinerea tensiunii arteriale (este cel mai important mecanism compensator
care permite ca pierderi de până la 20% din VSCE să nu se însoţească de modificări ale
tensiunii arteriale=
– într-o a doua etapă (o pierdere de ≥20 % din volumul sanguin circulant efectiv) intră în
acţiune baroreceptorii de înaltă presiune (sino-carotidieni, arc aortic, splahne) care
amplifică RSA cu creşterea eliberării de catecolamine care prin acţiune β1 vor produce
tahicardie, creşterea contractilitatii, etc., iar prin acţiune pe receptorii α-adrenergici vor
produce arteriolo-constricţie.
SOCUL si REACTIA HIPODINAMICA
Reacţia hipodinamică poate fi generată prin scăderea volumului sanguin circulant ca în şocul hipovolemic (scade presarcina
şi apoi debitul cardiac), sau prin scăderea primară a debitului cardiac ca în şocul cardiogen.
Macrocirculaţie:
- activarea baroreceptorilor şi declanşarea reacţiei simpato-adrenergice (RSA) cu eliberarea de
catecolamine la nivelul terminaţiilor libere simpatice şi a medulosuprarenalei.

Rezultate :
1 . creşterea eliberării de catecolamine care prin acţiune pe receptorii α-adrenergici vor produce intai
venoconstrictie apoi, arteriolo-constricţie iar pe β1 vor produce tahicardie, creşterea contractilitatii.

2. redistribuţia regională a fluxului sanguin (denumită în tratatele mai vechi „centralizarea circulaţiei”) dinspre organele
bogate în receptori alfa (splahne, muşchi scheletici, piele) înspre organele sărace în aceşti receptori (creier, cord)

3. activarea axului renină-angiotensina şi vasopresina vor creşte şi ele tonusul vasomotor, în special în patul vascular
mezenteric. (Angiotensina II va creşte eliberarea de aldosteron şi descărcările simpatice iar
Vasopresina va stimula atât eliberarera de catecolamine cât şi contractilitatea miocardică).

[Fluxul (debitul) = Presiune / rezistenţă]

TAM = DC x RVS
4. În final, ischemia celulară poate facilita reacţii de tip umoral şi proinflamator cu eliberare de mediatori (citokine, oxid
nitric,etc.) care vor agrava tulburările circulatorii ducând în final la leziune de organ şi moarte.
La nivelul microcirculaţiei, modificările macrocirculaţiei vor
induce următoarele fenomene care perturbă fiziologia capilară:
     modificări ale schimburilor capilare cu ţesuturile;
     maldistribuţie;
     şunt arterio-venos;
     modificări reologice;
     modificări structurale ale endoteliului capilar (care atunci
când sunt ireversibile compromit teritoriul dependent de ele). 
 Patternul hemodinamic al reacţiei hipodinamice şi al
şocului hipodinamic se caracterizează prin:

► macrocirculaţie:

1. Debit (DC) sau index cardiac (IC) scăzut

2. Rezistenţe vasculare sistemice (RVS) crescute

3. Presiuni de umplere
- în şocul hipovolemic presiunile de umplere (PVC, PCP) sunt mult scăzute
- în şocul cardiogen acestea sunt mult crescute.

►microcirculaţie : ∆(a-v)O2 crescută

 Hypovolemic Shock

• It is the most common cause of shock in trauma patients.

• Causes:
– External: bleeding (trauma), GI bleeding, ruptured
aneurysms, hemorrhagic pancreatitis. vomiting or
diarrhea, adrenal insufficiency, diabetes insipidus,
dehydration
– Internal: third spacing: intestinal obstruction, pancreatitis,
cirrhosis
Şocul cardiogen este o formă extremă de insuficienţă cardiacă
congestivă caracterizată prin următorul tablou hemodinamic:
-hipotensiune arterială (TA sistolică < 90 mm Hg sau scăderea TA
sistolice cu > 30% din valoarea iniţială)
-IC < 1,8 l/min/m2
-PCP > 22 mm Hg.

   
IC
I Normal II Congestie
(ml / min / m )
2
  pulmonară  
2,5
III Hipovolemie IV Insuficienţă
 
Cardiacă
Congestivă
 

0 18
PCP (mm Hg)
Definition SHOCK

Definition of shock :
- does not require the presence of hypotension.
- requires to prove “failure to deliver and/or utilize adequate amounts of O2”
and may include, but is not limited to, the presence of hypotension.

• Shock = circulatory and cellular dysfunction, manifested by markers of

hypoperfusion ( such as elevated blood lactate, decreased ScvO2 or SvO2), with
or without hypotension.
Definition
We recommend that shock be
defined as a lifethreatening,
generalized maldistribution of blood
flow resulting in failure to deliver
and/or utilize adequate amounts of
oxygen, leading to tissue dysoxia.
1B
Shock is best defined as a life-
threatening, generalized form of
acute circulatory failure associated
with inadequate oxygen utilization by
the cells. Ungraded - Definition
• It is a state in which the circulation is unable to
deliver sufficient oxygen to meet the demands
of the tissues, resulting in cellular dysfunction.
• The result is cellular dysoxia, i.e. the loss of the
physiological independence between oxygen
deliveryand oxygen consumption, associated
with increased lactate levels.
both: ungraded (UG), statments of facts(SF)
 Diagnosis of shock

• The diagnosis of acute circulatory failure is based on a combination of:

- clinical
- hemodynamic SIGNS
- biochemical
 CLINICAL SIGNS of SHOCK
• Hypotension ( not always present )
2014 +
Signs of altered tissue perfusion
visualized through the 3 ‘windows’ of the body :
- the peripheral window (skin that is cold, clammy and blue, pale or
discolored)

- the renal window (decreased urine output: < 0.5 mL/kg/h)

- the neurologic window (altered mental: obtundation, disorientation,

confusion)
 Hypotension & Shock
• SBP < 95 mmHg: sensitivity of 13% for moderate blood loss
sensitivity of 33% for severe blood loss

Stern SA et al. Ann Emerg Med 1993:155

• preserved blood pressure can be associated with markers of inadequate tissue

perfusion, such as decreased ScvO2 and significantly increased blood lactate

Rivers E & al: N Eng J Med 2001: 345:1368–1377

2014

1B
 Perfusion markers
- it exists a critical level of DO2 when VO2 becomes dependent on DO2 and:
LACTATE ↑ and regional and microcirculatory perfusion is ↓

• duration and area under the curve of the increased blood lactate levels have been
related to morbidity and mortality in different groups of pts. and have a place in
risk-stratification
Jansen TC, van Bommel J, Bakker J: Crit Care Med 2009, 37(10):2827–39
Bakker J, Gris P, Coffernils M, Kahn RJ, Vincent JL: Am J Surg 1996, 171(2):221–26.
Jansen TC, van Bommel J, Woodward RG, Bakker J: Crit Care Med 2009, 37(8):2369–74

• in the early phase of resuscitation, lactate levels is more closely related to outcome
than frequently used haemodynamics, including DO2 or VO2.

Jansen TC, van Bommel J, Mulder PG, Rommes JH: Crit Care 2008, 12(6):R160.
Bakker J, Coffernils M, Leon M, Gris P, Vincent J-L: Chest 1991, 99(4):956–962.
Howell M, Donnino M, Clardy P, Talmor D, Shapiro N: Intensive Care Med 2007, 33(11):1892–99.
Shapiro NI, Howell MD, Talmor D, Nathanson LA, Wolfe R: Ann Emerg Med 2005,45(5):524-28

• the usual cut-off value is 2 mEq/L (or mmol/L), but lactate levels > 1.5 mmol/L in
patients with septic shock are associated with increased mortality
Wacharasint P, Nakada TA, Boyd JH, Russell JA, Walley KR: Shock, 2012, 38:4–10
 Lactate, SvO2, ScvO2, ΔP(v-a)CO2
• We recommend arterial and CVC insertion in shock not responsive to initial
therapy and/or requiring vasopressor infusion. UG-BP

• We recommend measuring blood lactate levels in all cases where shock is

suspected. 1 C

• Lactate levels are typically2 > mEq/L (or mmol/L) in shock states. SF

• We recommend serial measurements of blood lactate: to guide, monitor and

assess. (every 2 h in the first 8 h and every 8–12 h thereafter) 1 C

• in pts. with a CVC we suggest measurements of ScvO2 and venoarterial

difference in PCO2 (VApCO2) to help assess the underlying pattern and the
adequacy of cardiac output as well as to guide therapy. 2 B

!!!!! ScvO2 ( cut off 70% Rivers) – SvO2 - PCO2 gap

Reacţia hiperdinamică se caracterizează din punct de vedere
hemodinamic astfel:
► macrocirculaţie:
- debit cardiac (DC|), index cardiac (IC) crescut;
- Rezistenţe vasculare sistemice (RVS) scăzute;
- presiuni de umplere (PVC, PCP) normale sau uşor scăzute.

 ►microcirculaţie :
- ∆(a-v)O2 normală sau la limita de jos;
- flux sanguin circulator periferic crescut, dar maldistribuit.
REACTIA
SISTEMICA = RASPUNS
POSTAGRESIUNE – neurohumoral
– metabolic
– imunologic
– celular
specific
RASPUNS
AGRESIUNE nespecific – generalizat la o agresiune majora
– INFECTIA
– TRAUMA
– HEMORAGIE – HIPOVOLEMIE
– ARSURA
– ISCHEMIE PRELUNGITA
– INTERV. CHIRURGICALA
stereotip
RASPUNS generalizat
nespecific
• central
• periferic
•
~ amploarea agresiunii
 SEPTIC SHOCK
• ACTIVATORI

• MEDIATORI
Elementele umorale ale raspunsului inflamator
March 2016

• JAMA. 2016;315(8):762-774. doi:10.1001/jama.2016.0288

• JAMA. 2016;315(8):775-787. doi:10.1001/jama.2016.0289

• JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287

 WHY these 3 Papers ?

• Sepsis = a syndrome of physiologic, pathologic, and biochemical

abnormalities induced by infection

• a major public health concern, accounting for more than $20

billion (5.2%) of total US hospital costs in 2011
Torio CM & Andrews RM.. Statistical Brief #160. 2011

• although the true incidence is unknown, conservative estimates

indicate that sepsis is a leading cause of mortality and critical
illness worldwide!
 Recommendations (1)
Definition of Sepsis

Sepsis is defined as life-threatening organ dysfunction

caused by a dysregulate host response to infection !
• elimination of the terms sepsis syndrome, septicemia, and severe sepsis

• this new definition emphasizes :

- the primacy of the non-homeostatic host response to infection
- the potential lethality that is considerably in excess of a straightforward
infection
- the need for urgent recognition.

Even a modest degree of organ dysfunction when infection is first

suspected is associated with hospital mortality in excess of 10% !
 Recommendations (2)
• Nonspecific SIRS criteria such as pyrexia or neutrophilia will continue to aid
in the general diagnosis of infection.

• SIRS criteria complement features of specific infections (eg, rash, lung

consolidation, dysuria, peritonitis) that focus attention toward the likely
anatomical source and infecting organism.

• However, SIRS may simply reflect an appropriate host response that is

frequently adaptive !

• Sepsis involves organ dysfunction, indicating a pathobiology more

complex than infection plus SIRS alone !

- “severe sepsis” becomes superfluous and redundant

- Sepsis need greater levels of monitoring, intervention and possible ICU admission.
 Results/Recommendations (2)
Clinical Criteria to Identify Patients With Sepsis

• SOFA score is intended to be used as a means to clinically

characterize a septic patient !

• a change in baseline of the total SOFA score of ≥ 2 points = organ dysfunction !

• the baseline SOFA score should be assumed to be 0 unless the patient is known to
have preexisting (acute or chronic) organ dysfunction before the onset of infection

• pts. with a SOFA score of ≥ 2 had an overall mortality risk of approximately 10% in
a general hospital population with presumed infection ( vs 8.1 % in STEMI ! )

• depending on a patient’s baseline level of risk, a SOFA score of ≥ 2 identified a

2- to 25-fold increased risk o dying compared with patients with a SOFA score less
than 2 points.
SOFA score
SOFA score & MORTALITY
 Definition of Septic Shock

• Septic shock is defined as a subset of sepsis in which

underlying circulatory and cellular metabolism
abnormalities are profound enough and are associated
with a greater risk of mortality than sepsis alone !

• The 2001 task force definitions described septic shock as “a state of

acute circulatory failure”

• The 2016 task force favored a broader view to differentiate septic

shock from cardiovascular dysfunction alone and to recognize the
importance of cellular abnormalities
Clinical Criteria to identify Septic Shock

Adult pts. with septic shock can be identified using the clinical criteria:

SEPSIS
and
• hypotension requiring vasopressors to maintain MAP≥65mmHg
and
• serum lactate level >2 mmol/L after adequate fluid resuscitation

With these combination criteria hospital mortality is >

40% !
 KEY MESSAGES (1)
• Sepsis : a life-threatening organ dysfunction caused by a dysregulated host
response to infection.

• For clinical use: organ dysfunction can be represented by an increase in (SOFA)

score of 2 points or more ( associated with an in-hospital mortality > 10%)

• Septic shock: a subset of sepsis in which particularly profound circulatory, cellular,

and metabolic abnormalities are associated with a greater risk of mortality than
with sepsis alone.
SEPSIS
and
• hypotension requiring vasopressors to maintain MAP≥65mmHg
and
• serum lactate level >2 mmol/L after adequate fluid resuscitation ( absence of
hypovolemia)

(hospital mortality rates greater than 40%)

 KEY MESSAGES (2)
• in out-of-hospital, emergency department, or general hospital ward settings

• adult patients with suspected infection can be rapidly identified as being more
likely to have poor outcomes typical of sepsis if they have:

at least 2 of the following clinical criteria

- altered mentation
- Systolic Blood Pressure of 100mmHg or less
- respiratory rate of 22/min or greater

namely:

quick SOFA Score ≥ 2

Cu ajutorul monitorizării hemodinamice invazive se pot descrie două clase ale
ICCac.:
 
- ICC ac. medie:  IC < 2,5 l/min/m2
 18 mm Hg < PCP < 22 mm Hg
 - ICC ac. severă:  IC < 2,5 l/min/m2
 PCP > 22 mm Hg
 normo/hipotensiune arterială
 
 Şocul cardiogen este o formă extremă de ICC ac. fiind caracterizat de:
 
-hipotensiune arterială (TA sistolică < 90 mm Hg sau scăderea TA cu > 30% din
valoarea iniţială)
-IC < 1,8 l/min/m2
-PCP > 22 mm Hg.
Şocul cardiogen este o formă extremă de insuficienţă cardiacă
congestivă caracterizată prin următorul tablou hemodinamic:
-hipotensiune arterială (TA sistolică < 90 mm Hg sau scăderea TA
sistolice cu > 30% din valoarea iniţială)
-IC < 1,8 l/min/m2
-PCP > 22 mm Hg.

   
IC
I Normal II Congestie
(ml / min / m )
2
  pulmonară  
2,5
III Hipovolemie IV Insuficienţă
 
Cardiacă
Congestivă
 

0 18
PCP (mm Hg)
 TRATAMENT SOC HIPOVOLEMIC

Restabilire DO2
1. VOLEMIE
2. Transportor (Hb) PULM
3. Optimizare functie
4. trat. reologic CARDIACA

TRATAMENT SOC CARDIOGEN

Restabilire DO2 DC
1. Mentinerea TAS NORADRENALINA
2. Trat. etiologic IMac
Valv
DSV
TR
Tamponada
embolie pulm
3. Trat. asociat
 TRATAMENT SOC SEPTIC

1. TRAT. ETIOLOGIC
— plaga, trauma, arsura
— focar septic
— antibiotice
— Ac monoclonali
2. Trat. PATOGENIC
• Proteina C activata
• CORTIZON
• CYTOSORBENTS !
• Vitamin K ?
3. Trat. la nivel ORGAN – SISTEM
OPTIMIZARE FUNCTIE
— Cardiovasculara
— Pulmonara
— Renala
— Metabolica
— Nutritie
PROTEZARE
 m
• m
 74 pages , 655 references: only for ADULTS

SSC 2017 provides 93 statements:

(early management and resuscitation of pts. with sepsis or septic shock)
- 32 strong recommendations
- 39 weak recommendations
- 18 BPS (best-practice statements)
- 4 questions: No recommendation

The panel consisted of five sections:

1.Hemodynamics
2. Infection
3. Adjunctive therapies
4. Metabolic
5. Ventilation
NEW

NEW
NEW
!
 I.BLOOD PRODUCTS

J. IMMUNOGLOBULINS

K. BLOOD PURIFICATION

L. ANTICOAGULANTS

M. MECHANICAL VENTILATION

N. SEDATION AND ANALGESIA

O. GLUCOSE CONTROL

P. RENAL REPLACEMENT THERAPY

Q. BICARBONATE THERAPY

R. VENOUS THROMBOEMBOLISM PROPHYLAXIS

S. STRESS ULCER PROPHYLAXIS

T. NUTRITION

U. SETTING GOALS OF CARE

 D. ANTIMICROBIAL THERAPY

9 recommendations in 2012 : 15 recommendations in 2016

1
 SOCUL ANAFILACTIC

I. R. anafilactica = interactiune Ag – Ac
II. R. anafilactoida = eliberare directa de mediator din mastocit

Clinic – LA FEL!
FIZIOPAT.
Complex Ag – Ac (IgE)
sau activare
direct Mastocit
Bazofil

Elib. MEDIATORI
PRIMARI / SEC

AMPc
GMPc
 SOCUL ANAFILACTIC
Med primari
– HISTAMINA
– compl SRSA
– PAF, PG, LTB4

Med secundari
– C3a, C5a
– C7a + C8a + C9a = C. ATAC
– f XIIa
– Kinine- ~
CLINIC sever!
Dispnee, Eruptie, Angioedem
Bronhospasm – hTA – EPA
ACIDOZA LACTICA Soc hipovolemic STOP CR
• hipovolemie
• vasodilatatie
• contract. mioc.
• modif. permeab. PULM
Tratament 1. Terapie respiratorie
2. catecolamine / ADRE !!!
3. hipovolemie
4. antihistaminice
5. cortizon
 SOCUL NEUROGEN

TRAUMA SNC
Cauza hTA
RAHIANESTEZIE

Fiziopat: disfunctie acuta S.N.Sy

SIMPATICOLIZA

hipotalamus maduva cerv-tor

tr. cerebral
vasodilatatie + bradicardie
RVS
intoarcerii venoase
hTA DC
Tratament Simpatomimetice (tonus Sy)
Volemie
 LEAK
CAPILAR
HIPOVOLEMIC

↓RVS
↑DC

MALDISTRIBUŢIE A EXTRACARDIAC
MICROCIRCULAŢIEI ↓DC OBSTRUCTIV
↑RVS
DISTRIBUTIV

↓PAM
HIPOPERFUZIE ↓ PERFUZIA
TISULARĂ DEPRESIE CORONARIANĂ
MIOCARDICĂ
ŞOC

INJURIE
CELULARĂ CARDIOGEN
MICROTROMBOZE
MODS

CLEARANCE-UL
TOXICELOR
ACIDOZA
MEDIATORI
Leziuni ale
barierei intestinale