Prof.dr.erban Bubenek MD
Physiology of Cardiovascular System
CO = SV x HR (Normal = 4.0 - 8.0 l/min)
MAP = CO x SVR
VO2 = DC ( CaO2-CvO2)
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
CvO2 CaO2
DO2
CaO2
VO2
SHOCK
1743 Henri Francois Le Dron
DO2 VO2
PRecharge ( hypovolemic S. ) SEPTIC SHOCK
CO CO
Contractility (cardiogenic S. )
- PR, Contr + Postcharge (a Hyperdinamic form of shock )
(obstructive shock)
3 are hypodinamic forms of shock
all
+: 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
4. Minimalizarea durerii
-Nespecific
5. Vindecarea plagii
- Generalizat
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
Macrocirculaie:
- activarea baroreceptorilor i declanarea reaciei simpato-adrenergice (RSA) cu
eliberarea de catecolamine la nivelul terminaiilor libere simpatice i a
medulosuprarenalei.
n dou etape:
Rezultate :
1 . creterea eliberrii de catecolamine care prin aciune pe receptorii -adrenergici vor produce intai
venoconstrictie apoi, arteriolo-constricie iar pe 1 vor produce tahicardie, creterea contractilitatii.
2. redistribuia regional a fluxului sanguin (denumit n tratatele mai vechi centralizarea circulaiei) dinspre organele
bogate n receptori alfa (splahne, muchi scheletici, piele) nspre organele srace n aceti receptori (creier, cord)
3. activarea axului renin-angiotensina i vasopresina vor crete i ele tonusul vasomotor, n special n patul vascular
mezenteric. (Angiotensina II va crete eliberarea de aldosteron i descrcrile simpatice iar
Vasopresina va stimula att eliberarera de catecolamine ct i contractilitatea miocardic).
macrocirculaie:
3. Presiuni de umplere
- n ocul hipovolemic presiunile de umplere (PVC, PCP) sunt mult sczute
- n ocul cardiogen acestea sunt mult crescute.
IC
I Normal II Congestie
(ml / min / m2) pulmonar
2,5
III Hipovolemie IV Insuficien
Cardiac
Congestiv
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.
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):282739
Bakker J, Gris P, Coffernils M, Kahn RJ, Vincent JL: Am J Surg 1996, 171(2):22126.
Jansen TC, van Bommel J, Woodward RG, Bakker J: Crit Care Med 2009, 37(8):236974
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):956962.
Howell M, Donnino M, Clardy P, Talmor D, Shapiro N: Intensive Care Med 2007, 33(11):189299.
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, 38:410
Lactate, SvO2, ScvO2, P(v-a)CO2
Lactate levels are typically2 > mEq/L (or mmol/L) in shock states. SF
microcirculaie :
- (a-v)O2 normal 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
- Sepsis need greater levels of monitoring, intervention and possible ICU admission.
Results/Recommendations (2)
Clinical Criteria to Identify Patients With Sepsis
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 ! )
Adult pts. with septic shock can be identified using the clinical criteria:
SEPSIS
and
hypotension requiring vasopressors to maintain MAP65mmHg
and
serum lactate level >2 mmol/L after adequate fluid resuscitation
adult patients with suspected infection can be rapidly identified as being more
likely to have poor outcomes typical of sepsis if they have:
namely:
ocul cardiogen este o form extrem de ICC ac. fiind caracterizat de:
-hipotensiune arterial (TA sistolic < 90 mm Hg sau scderea TA cu > 30% din
valoarea iniial)
-IC < 1,8 l/min/m2
-PCP > 22 mm Hg.
ocul cardiogen este o form extrem de insuficien cardiac
congestiv caracterizat prin urmtorul tablou hemodinamic:
-hipotensiune arterial (TA sistolic < 90 mm Hg sau scderea TA
sistolice cu > 30% din valoarea iniial)
-IC < 1,8 l/min/m2
-PCP > 22 mm Hg.
IC
I Normal II Congestie
(ml / min / m2) pulmonar
2,5
III Hipovolemie IV Insuficien
Cardiac
Congestiv
0 18
PCP (mm Hg)
TRATAMENT SOC HIPOVOLEMIC
Restabilire DO2
1. VOLEMIE
2. Transportor (Hb) PULM
3. Optimizare functie
4. trat. reologic CARDIACA
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
NEW
NEW
!
I.BLOOD PRODUCTS
J. IMMUNOGLOBULINS
K. BLOOD PURIFICATION
L. ANTICOAGULANTS
M. MECHANICAL VENTILATION
Q. BICARBONATE THERAPY
T. NUTRITION
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
SIMPATICOLIZA
RVS
DC
MALDISTRIBUIE A EXTRACARDIAC
MICROCIRCULAIEI DC OBSTRUCTIV
RVS
DISTRIBUTIV
PAM
HIPOPERFUZIE PERFUZIA
TISULAR DEPRESIE CORONARIAN
MIOCARDIC
OC
INJURIE
CELULAR CARDIOGEN
MICROTROMBOZE
MODS
CLEARANCE-UL
TOXICELOR
ACIDOZA
MEDIATORI
Leziuni ale
barierei intestinale