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Definition of Shock

Inadequate oxygenation or

perfusion causes:

Inadequate cellular oxygenation

Shift from aerobic to anaerobic

metabolism

Shock is a major critical illness that

involves almost every organ system. It is

not simply a problem of decreased blood

pressure. Rather, it is a problem of

inadequate tissue perfusion and

oxygenation (Rice,1991)

.syok merupakan keadaan sakit kritis berat yang

mengakibatkan perburukan pada hampir setiap

sistem organ, masalahnya tidak sesederhana berupa

penurunan tekanan darah. Melainkan problem tidak

kuatnya perfusi dan oksigenasi jaringan..


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Definisi

Hipotensi

Tekanan Darah Sistolik < 90 mmHg

Tekanan Darah Sistolik berkurang > 40 mmHg

Hipoperfusi

Perubahan status mental

Oliguria

Asidosis

defisit basa > 2

laktat > 2.5 mmol/L


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Syok Hipovolemik

Syok yg disebabkan krn tubuhkehilangan darah, plasma atau cairantubuh yg lain

Misalkan : pembedahan, trauma, lukabakar atau muntah & diare

.... Syok akibat perdarahan syokyang paling umum pada pasientrauma/cidera

(..terutama pada pasien dengan multiple trauma, fraktur tulang2 panjang/pelvis,trauma dengan ruptur/perdarahan organ di rongga abdomen, >> kadar hematokrit& hemoglobin tidak dapat menjadi parameter berat ringanya perdarahan padaperdarahan akut/mendadak)

Kehilangan bentuk lain spt peritonitis,pancreatitis, obstruksi ileus (third space)


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Blood Flow ????

Keadekuatan aliran darah

dipengaruhi oleh :

Pompa jantung yg adekuat

vaskulator/sistem sirkulasi ygefektif

Volume darah yg adekuat

Bila salah satu komponenterganggu/rusak

syok>>kematian

..CO = SV x SVR


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Blood pressure Tissue perfusion

Cardiac output x Vascular resistance


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Faktor yg Mempengaruhi Stroke

Volume

1. Pre-Load: volume pengembalian darahke jantung ** ... Dipengaruhi oleh pengisian vena,keadaan volume darah & perbedaan antara tekanan

sistemik vena serta tekanan atrium kanan

2. Kontraktilitas jantung: kemampuanjantung dlm memompaHk. Starling

3. After load: tahanan pembuluh darah

perifer/sistemik


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SIRKULASI PEMBULUH DARAH ARTERI & VENA


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Breathing (ventilation): air in to andout of lungs

External respiration: gas exchange

between air and blood

Internal respiration:gas exchange

between blood and tissues Cellular respiration: oxygen use to

produce ATP, carbon dioxide as

waste

Four Respiration Processes


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Oxygen delivery/DO2= HR X SVX Hb X S02 X 1.39 + 0.03 X PaO

Cardiacoutput Arterial O2content

DO2= COx CaO2


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Pathogenesis

Hypoperfusi

Met. Anaerob

ATP

Na+ pump #

Apoptosis


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Hypovolaemia and Shock

decreased blood volumedecreased cardiac output

decreased oxygen delivery

impaired macrocirculation

vasoconstriction

Inadequate perfusionErythrocyte aggregation

impaired micro circulation

tissue ischemia organ failure

kidney

bowel

endotoxinrelease

septic shock

Shock Cascade in Haemorrhage


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Impaired Oxidative

Metabolism Hypoperfusion Free radical

Inflammatory Mediators Impair mitochondria function

Fink , P. M 2005


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.....respon selular terhadap syok

Respon seluler : akibat oksigenasi yang rendahmetabolisme anaerob >> asam laktat asidosismetabolik....

Bila semakin parah (..prolong syok) maka membransel rusak dan kehilangan fungsi

....retikulum endoplasma membengkak, lisosompecah dan mengeluarkan enzim yang dapat merusaksel... terjadi edema dan kematian sel


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Organ Dysfunctions

Ischemic injury related to tissuehypoperfusion ;

MAP < 60 mmHg result ischemic injury,

anaerobic metabolism productions high-energy phosphate bellow level for cellularfunction and membrane integrity

Mediator related 0rgandysfunctionsReperfusion Injury


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MENGENAL SYOK

Tanda syok yg didapatkan mrpk reaksikompensasi tubuh terhadap syok

Respon dini : tachicardia & vasoconstrictikulit

Mrpk kompensasi utk menjaminaliran/perfusi darah ke otak, jantung & ginjal

Kompensasi ini dpt mencegah penurunandarah sistolik meskipun penderita telah

kehilangan 30 % vol darahhrs diperhatikan jg tanda & gejala klinis syokyg lain


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Syok Phase

1. Compensatory phase

2. Progresive phase

3. Irreversible phase


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Temuan Klinis Berdasarkan Fase

Syok

Kompen

sasi

Progresif Irreversibel

HR > 100

x/mnt

> 150x/mnt Eratik/sistol

TD Normal TDS < 80-90

mmHg

Mbthkan dukungan

mekanik &

farmakologis

RR >20 Cepat,

dangkal,

Krekels

Membutuhkan

intubasi


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Kulit Dingin,

kusam

Bercak,

ptekie

Ikterik

Urin

output

Menurun


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Tanda & Gejala Syok

Respiratory system

nafas cepat & dangkal

Circulation system

Ekstremitas pucat, dingin & berkeringat dingin

Nadi cepat & lemah

CRT > 2 detik

TD turun bila kehilangan darah mencapai 30 %

Vena tampak kolaps


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Sistem saraf pusat

Keadaan mental/kesadaran tergantung

derajat syok

Dimulai gelisah/bingung sampai tdk sadar

Sistem ginjalproduksi urin menurun

Sistem pencernaanmual & muntah

Sistem kulit & otot

Turgor menurun

Mata cekung

Mukosa & lidah kering


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Kelas I Kelas II Kelas III Kelas IV

Kehilangan darah(ml)

Sampai 750 750-1500 1500-2000 >2000

Kehilangandarah(%vol.darah)

Sampai 15 % 15 % - 30 % 30 % - 40 % > 40 %

Denyut nadi < 100 >100 >120 >140

Tek. Darah Normal Normal Menurun Menurun

Tek. Nadi Normal/naik Menurun Menurun Menurun

Frek. Nafas 14-20 20-30 30-40 >35

Prod. Urin(ml/jam)

>30 20-30 5-15 Tdk berarti

Status CNS/status mental

Sedikit cemas Agak cemas Cemas, bingung Bingung, lesu(lethargic)

Penggantiancairan (hk. 3 : 1) Kristaloid Kristaloid Kristaloid &darah Kristaloid &darah


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Hubungan antara derajat perdarahan dengan

kematian sel


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Critical Oxygen Delivery


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Course of hypovolemic shock inabsence of therapy

Decompen-sation

Compen-sation

Bleeding

Heart rate

min

Blood pressure mmHg

Irreversi-bility

Three Shock phases

Bloodpressure

0

50

100

150


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Jika terjadi perdarahan yang sangat banyak, dan jantung

tidak mampu memperbaiki aliran darah ke jaringan

produksi asam laktatmenurunkan pHa menurunnya

afinitas Hb-O2meningkatkan transport oksigen ke

jaringan hipoksik (pergeseran kurva disosiasi ke kanan)


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Tabel Respon Thd Pemberian Cairan Awal

Respon cepat Respon

sementara

Tanpa respon

Tanda vital Kembali ke normal Perbaikan sementara

Tensi & nadi kembaliturun

Tetap abnormal

Dugaan kehil.Darah

Minimal (10 % - 20%)

Sedang, msh ada (20% - 40 %)

Berat (>40%)

Kebutuhankristaloid

Sedikit Banyak Banyak

Kebutuhan darah Sedikit Sedang-banyak Segera

Persiapan darah Tipe spesifik &

crossmatch

Tipe spesifik Emergensi

Operasi Mungkin Sangat mungkin Hampir pasti

Kehadiran dini ahlibedah

Perlu Perlu perlu

Ringer Laktat 2000 cc pd dewasa, 20 CC/Kg BB pd anak-anak


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TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERY

Oxygen delivery/DO2= HR X SVX Hb X S02 X 1.39 + 0.03 X PaO

Cardiacoutput

Arterial O2

content

FluidsTransfuse Partially

dependent onFIO2and

pulmonarystatus

Inotropes :Dopamin

Dobutamin

Norepinephrin

Epinephrin

DO2= COx CaO2


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Therapeutic Goals in Shock

Control of bleeding

establish adequate ventilation and oxygenation

Restoration blood volume

Increase O2 delivery

Optimize O2 content of blood

Improve cardiac output and

blood pressure

Match systemic O2 needs with O2 delivery Reverse/prevent organ hypoperfusion


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Goals for fluid resuscitation

Maintenance or achievement of normovolemia

and hemodynamic stability

Restitution of fluid balance between the different

fluid compartments

Maintenance of an adequate colloid oncotic

pressure Enhancement of microvascular bloodflow


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End points of resuscitation

Basic clinical signs

Heart rate

Blood pressure

Urine output

Capillary refill Monitor for deterioration of oxygenation


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RL

RANaCl 0.9 %

NaCl 3 %

Albumin

PlasmaDextran

Gelatin

HES

COLLOIDCRYSTALLOID

B

LO

O

D


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What do you replace with?

Crystalloid

4.1 x blood loss

Colloid*

1.4 x blood loss


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Body Fluid Compartments

Total body water = 60 % of body weight (BW)

2/3

Intracellular water= 40 % of BW

1/3

Extracellularwater

= 20 % of BW

Plasma (5 % of BW)

Extracellularwater

= 20 % of BW


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KRISTALOID

Keuntungan

Komposisi elektrolit seimbang

Tidak ada resiko alergi

Tidak mempengaruhi hemostasis

Mengakibatkan terjadinya diuresis

Murah


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Kerugian

Perlu 3-4 x jumlah perdarahan

Bisa mengakibatkan edema

Mengakibatkan TOP berkurang.

Hypothermia

Lama kerja + 90 menit

NaCl 0.9% : asidosis hiperchloremia

KRISTALOID


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KOLOID

KEUNTUNGAN

Tetap berada dalam volume

intravaskular

Kebutuhan sama denganjumlah darah yang hilang

Meningkatkan TOP

Resiko edema minimal

Meningkatkan aliran darah

microvaskular


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KERUGIAN

Kelebihan beban cairan

Mengganggu hemostasisMempengaruhi fungsi ginjal

Reaksi anafilaktoid

Mahal

KOLOID


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16 hr

16 hr

17 day

10 hr

6 hr

12 hr

0.7 1.3

4.0 5.0

1.0 1.3

1.5

1.0 1.5

0.8

20 mm Hg

70 Mm Hg

30 Mm Hg

40 Mm Hg

40 Mm Hg

40 Mm Hg

69.000

69.000

69.000

120.000

26.000

41.000

5 % ALBUMIN

25 % ALBUMIN

6 % HETASTARCH

10 % PENTASTARCH

10 % DEXTRAN-40

6 % DEXTRAN-70

SERUM

HALF-LIFE

PLASMA

VOLUME

EXPANSION***

ONCOTIC

PRESSURE**

AVERAGE

MOLECULAR

WEIGHT * (DALTONS)FLUID

CHARACTERISTICS OF INTRAVENOUSCOLLOID FLUIDS


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The History of Transfusion

Triggers

1980 the 10/30 rule

The American Society of Anesthesiology. 6-10,

g/dl

The American College of Physician. 8, g/dl

The National Institute of Health. 7, g/dl

The Transfusion Requirements in Critical Care.

7-9, g/dl


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ASA Practice Guidelines for Blood

transfusion

Rarely indicated if Hb > 10 gr%, alwaysindicated Hb < 6 gr% esp in acute anemia

If Hb between 6 - 10 gr%, indication of RBC

transfusion should be based on the patients risk forcomplication of inadequate oxygenation

Not recommended to use a single Hb trigger

for all patients, without considering allimportant physiologic & surgical factors

affecting oxygenation

Postoperati e O tcomes of


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Postoperative Outcomes of

Anemic Jehovahs Witnesses

Addison K M et al. Rational use of blood production in : Lanten PN ed the intensive care unit manual

2001. P181-92

Preoperative HemoglobinLevel

Mortality

10 g/dl 7.1 %


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Anemia is tolerated better thanHypovolemia

Allows the initial fluid resuscitation

to be non Blood


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Oxygen Delivery= CO x CaO2

CO (SVxHR) xCaO2 (Hb x SpO2 x 1,39 + 0,003xPaO2)

CO= cardiac output CaO2= Oxygen content

Important determinant to tissue

oxygenationComponent : Cardiac Output, Hb,

SpO2 arterial & venous blood


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PENTING !

VOLUME INTRA-VASKULAR

O2 TRANSPORT ( ERITROSIT )

JUMLAH OKSIGEN YANG TERSEDIA UNTUK JARINGAN :

CO X (SAT.O2 X Hb X 1.39 + PO2 X 0.03)

= 5 l/m X 20 l/m O2/100 ml

= 1 liter O2/m

KEBUTUHAN = 25 % = 250 ml O2/m

Transfusion Guidelines for Unstable Patients Who Are


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Transfusion Guidelines for Unstable Patients Who Are

Acutely Bleeding

Addison K M et al. Rational use of blood product in : Lanken PN ed the intensive care unit manual2001. P181-92

Clinical situation Recommended response

Evidence of rapid acute

hemorrhage without immediate

control

Tranfuse PRBC

Estimated blood loss > 30-40%,

presence of symptoms of severeblood loss

Tranfuse PRBC

Estimated blood loss < 25-30%

without uncontrolled

hemorrhage

Crystalloid-colloid resuscitation,

proceed to blood transfusion if

recurrent signs of hypovolemia

Presence of comorbid factors Consider transfusion with lesser

degrees of blood loss

Evidence of rapid acute

hemorrhage or > 30-40% blood

loss

Requires emergent control of

bleeding source


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Guidelines for Blood Transfusions and management of

Blood Loss During the Perioperative period

Hb > 10 g/dL transfusions rarely indicated

Hb < 6 g/dL transfusions almost always indicated, especially whenthe anemia is acute

Hb 6 -10 g/dL decision to transfuse is determined by patients riskfor complications of decreased tissue oxygenation (patients with

ischemic heart disease)

Transfusion trigger : not recommended for application to all patients as itignores phsiologic and surgical factors to individual patients

Preoperatif autologous donation in selected patients

Intraoperatif blood salvage when appropiate

Acute normovolemic hemodilution when appropiate

(Stoelting,RK, 2002)


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PENUTUP

SHOCK MERUPAKAN KONDISI KRITIS (MENGANCAM

JIWA),

PRIORITAS PERTAMA YANG HARUS DILAKUKAN

ADALAH RESUSITASI

RUMUS RESUSITASI :

A B C D dst.

D : DRUGS & FLUIDS (resusitasi cairan)


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Lanjutan penutup

BODY FLUID, ELECTROLYTES AND ACID-BASE HAVE ACLOSED RELATION ONE TO ANOTHER

DISTURBANCE OF THE FLUIDS BALANCE HAS IMPACT

TO ELECTROLYTES AND ACID-BASE REGULATION

DALAM RESUSITASI CAIRAN PD SHOCK, JUGA MELIPUTI

MENORMALKAN KADAR ELEKTROLIT DAN

KESEIMBANGAN ASAM-BASA (HOMEOSTASIS MILLIEUINTERNA)


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Lanjutan Penutup . . .

Terapi diberikan atas dasar diagnosis

ditambah kesimpulan data2 monitoring.

(bukan menerapi jumlah/volume defisit

cairan dan angka-angka hasillaboratorium).

Eti l f i l t h k


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Etiology of circulatory shock

1.Hypovolemic - intravascular fluid volume loss

hemorrhage, fluid depletion or

sequestration

2.Cardiogenic - impairment of heart pump

myopathic lesions: myocardial

infarction, cardiomyopathies

dysrhythmias

obstructive and regurgitant lesionsofintracardial blood flow mechanics


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3.Obstructive - factors extrinsic to cardiac valves andmyocardium

v. cava obstruction, pericardialtamponade,

pulmonary embolism,

coarctation of aorta

4.Distributive - pathologic redistribution of intravascularfluid volume

septicaemia: endotoxic, secondary to

specific infectionanaphylactic

NORMAL


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NORMAL

1. HYPOVOLEMIC 2. CARDIOGENIC

3. DISTRIBUTIVE

High Resistance 4. OBSTRUCTIVELow Resistance

P th i f i l t h k


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Pathogenesis of circulatory shock

Usually results from inadequate cardiac output (CO)

Any factor reducing CO will likely lead to shock

2. Decreased venous return- diminished blood volumedecreased vasomotor tone- obstruction to blood flow at somepoints in the circulation

1. Cardiac abnormalitiesdecreased ability of the heart to pump blood

- myocardial infarction

- toxic states of heart- severe heart valve dysfunction- arrhythmias

Stages of shock


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Stages of shock

1. Nonprogressive stage (compensated)

Compensatory mechanisms (negative feedback)of the circulation canreturn CO and BP to normal levels

- baroreceptor reflexessympathetic stimulation constrict arteriols inmost parts of the body and venous reservoirs protection ofcoronary and cerebral blood flow

- angiotensin-aldosteron, ADH vasoconstriction,water and salt retention by the kidneys

- absorption of fluid from ISF and GIT, increased thirst

2. Progressive shock


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- positive feedback mechanisms are developed and cancausevicious circle of progressively decreasing CO

- circulatory system themselves begin to deteriorate,

without therapy shock becomes steadily worse until death

Cardiac depression -coronary blood flow, contractility

Vasomotor failure -cerebral blood flow

Release of toxins by ischemic tissues: histamine,serotonin, tissue enzymes

Intestines hypoperfusion mucosal barrier disturbance endotoxin formation and absorption vasodilatation, cardiac depression

Generalised cellular deterioration: K+ , ATP, release of hydrolases first signsof multiorgan failure

Vasodilation in precapillary bed


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3. Irreversible shock- despite therapy circulatory system continues to

deteriorate and death ensues

- marked hypoxic tissue damage

- endothelial dysfunction adhesive molecules,

neutrophils, macrophagesinflammation

- progressive acidosis

- advanced disseminated intravascular coagulation

- microcirculation failure plasma proteins leak

to interstitium

Cardiogenic shock


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Cardiogenic shock

- ventricle fails as a pump

- infarction process (45% loss of functional mass of

left ventricle)

- BP 90 torr for at least 30 min,pulmonary capillary pressure lung edema

- self-perpetuing cycle then ensues (vicious circle): metabolic acidosisandreduced coronary perfusionfurther impairing ventricular function andpredisposing to the development of dysrhythmias

Progression of myocardial dysfunction:

- hypotension, tachycardia, fluid retention, hypoxemia

Septic shock


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Septic shock

Typical causes: peritonitis, gangrenous infection, pyelonephritis

Special features:

1. high fever

2. marked vasodilatation (inflammation)

3. or normal CO: vazodilatation, metabolic rate

4. disseminated intravascular coagulation clotting factors tobe used up hemorrhages occur into many tissue (GIT)

IL-1 and TNF: PGE2, leukotrienes and NO

- vascular relaxation- endothelial permeability (deficit of intravascular volume)- myocardial contractility

Early stage:no signs of circulatory insufficiency


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Progression of infection:circulatory disorders becomes

Bacterial toxins deterioration of circulation end-stage is not greatly different from the end-stageof hemorrhagic shock (hypodynamic stage)

Death: - hypotension- multiorgan failure

Cell dysfunction


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Cell dysfunction

prolong tissue hypoperfusion cell membranelesion, lysosomal enzymes cell death

mechanisms:hypoxia, inflammatory mediators,free radicals


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Multiorgan failure

Kidney

- blood flow (to 10%) GF oliguria

- ischemia acute tubular necrosis

- countercurrent mechanism failure izostenuria

- marked lesions acute renal failure


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Lungs

- disturbances of pneumocytes andendothelium

- accumulation of Tr, Neu in pulmonarycirculation release of proteases

- leukotriens and free radicals- permeability - surfactant, edemaand hemorrhagies

respiratory insufficiency

(ARDS)


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25

50

75

100 % SURVIVAL

( 142 Pts)

0-1 1-2 2-3 3-4 4-6 6-11 11-16 > 16

LACTATE mM/l

HYPOVOLEMICEXTRACARDIAC

ObstructionCARDIOGENIC DISTRIBUTIVE


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HYPOVOLEMIC Obstruction

Fluid loss,

hemorrhage

e.g., Pericardial

tamponadeMyocardial

injury or

necrosis

Decreased

systemic

vascularresistance

Myocardiac

dysfunction

Reduced

systolic performance

Reduced

filling

Low cardiac

output

Reduced

preload

Decreased arterial

pressure

Shock

Multiple organ

system failure

High or normal

cardiac output

Maldistribution

of blood flow in

microcirculation


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