Myoung Soo Kim M.D. - gs.yonsei.ac.krgs.yonsei.ac.kr/download/Slide_shock_2003.pdf6 Pathophysiology of shock (4) C. Circulatory redistribution “For preservation of vital organ”

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ShockShockMyoung Soo Kim M.D.Myoung Soo Kim [email protected]@wonju.yonsei.ac.kr

http://myhome.hananet.net/~kim63http://myhome.hananet.net/~kim63

Department of SurgeryYonsei University Wonju College of Medicine

http://gs.yonsei.ac.kr

Definition of Shock

“ Syndrome that results from inadequate perfusion of tissues “

insufficient to meet the metabolic demands of those tissuealterations in cellular metabolism

: cellular dysfunction / elaboration of inflammatory mediators / cellular injury

multiple organ dysfunction syndrome(MODS) or frank organ failure

WCH-GS, 1998

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Classification of shock

Classification MechanismsAssociated

Clinical ConditionsHemorrhagic hemorrhagic loss trauma,

G-I bleeding,ruptured aneurysms

Hypovolemic

Plasma volume loss extravascular fluidsequestration

Pancreatitis, burns,bowel obstruction,excessive gastrointestinal loss

Intrinsic Infarction (MI),cardiomyopathy,valvular heart disease,

Cardiologic

Extrinsic

heart is unable togenerate an adequatecardiac output tomaintain tissue perfusion Compressive or obstructive

lesionNeurologic Failure of the sympathetic nervous system to

maintain normal vascular tone decreasedarteriolar and venous vasomotor tone

spinal cord injury,severe head injury,spinal anesthesia

Systemic inflammatoryresponse syndrome(SIRS)

(1) Infectious (septic) (2) Noninfectious

Septic shockSystemic Sepsis

Anaphylatic AnaphylaxisHypoadrenal Adrenal insufficiency

Vasogenic

Traumatic

Release ofendogenous orexogenous vasoactivemediators

Decreased arteriolarand venous vasomotortone

Trauma

Patient monitoring(1)

WCH-GS, 1998

Early treatment before irreversible tissue damageIdeal monitoring

= “monitoring of tissue and cell level perfusion”but the ideal monitoring is not possible

1. Conventional monitoring techniques ; based on physical examination or laboratory data

blood pressure, heart rate, central venous pressure, hematocrit, arterial blood gases, and urine output : more objective capillary refill, skin temperature, skin turgor

“ Poor relationship between index and clinical status”

" 그럼에도불구하고이러한 monitoring은초기 Shock치료의지표로유용하다"

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Patient monitoring(2)

2. Adjunctive monitoring techniques. : invasive / costly / potentially hazardous

1) Pulse oximetry2) Pulmonary artery catheterization - Swan-ganz catheter3) Mixed venous oximetry4) Continuous cardiac output monitoring5) Transcutaneous oxygen monitoring6) Serum lactate concentration7) Gastrointestinal tonometry

WCH-GS, 1998

Swan-Ganz Catheter

WCH-GS, 1998

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Pathophysiology of shock - overview

Shock syndrome = "Consequence of tissue hypoperfusion"

WCH-GS, 1998

Pathophysiology of shock (1)

A. Role of hypoxia

Primary pathophysiology of shock “impaired tissue hypoperfusion decreased oxygen

delivery relative to oxygen needs.”

WCH-GS, 1998

(1) supernormal level of oxygen delivery ? (2) significance of decreased O2ER and

increased SVO2

a. arteriovenous shunting, b. bioenergetic failurec.down-regulation

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B. Anaerobic metabolism and acidosis

WCH-GS, 1998

Anaerobic metabolism increased lactate production

decreased pyruvatehyperlactemia (> 2 mmol/L) and

blood lactate/pyruvate(L/P) ratio (>10)

Acidosis


WCH-GS, 1998

Mild acidemia(pH > 7.2) Severe acidemia(pH < 7.2)Catechol stimulation decreased responsiveness of catecholTachycardia,Increased cardiac output,Vasoconstriction

bradycardia,decreased cardiac outputvasodilation,direct negative inotropic effect ( slow

calcium ion flux)decreased threshold for ventricular

fibrillationright-ward shift of the oxyhemoglobin

dissociation curve

Clinical Signs of acidosis

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C. Circulatory redistribution

“For preservation of vital organ”

Mechanism of blood flow re-distribution

WCH-GS, 1998

Hypodynamic shock : Hypovolemic or cardiologic shock

Hyperdynamic shock : Vasogenic shock(sepsis state)

Vasoconstrictive effect increase in systemic vascularresistance(especially splanchnic vascular R)

Reduction in systemic vascular resistance

Vasoconstrictive factor : Catechols, angiotensin II, Vasopressin, endothelin, thromboxan A2.

Vasodilatory mediators: Nitric oxide, prostaglandin E2, Prostacyclin, interleukin-2, bradykinin

Redistributionof blood flow Splanchnic (G-I tissue) ischemia

Maldistribution of blood flow well-perfused regions vs. ischemic region


D. Role of the gut in shock

“Effect and Cause of Shock”

WCH-GS, 1998

(1) hypoxic injury Mucosal ischemia disruption of thenormal epithelial cell barrier1) cellular injury by the process of lipidperoxidation disruption of cellmembrane integrity.

(2) reperfusion injury accumulation of toxic oxidants(superoxide anion(O2ㆍ),hydroxy radical(OHㆍ) andhydrogen peroxide(H2O2))

2) chemotactic role : tumor necrosisfactor-alpha(TNF-α), platelet activatingfactor(PAF), interleukin(IL)-1 and IL-6,and others

Intestinal mucosal injuryIncreased permeabilityTranslocation of gut

bacterial and toxinmaterial

amplify SIR andMODS

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Mediators of Shock and Sepsis -overview

1) Endotoxin 2) Complement Fragments3) Eicosanoids 4) Kinins5) Nitric oxide6) Cytokines7) Platelet activating factor8) Endogenous opioids9) Oxidants

10) Neuroendocrine mediators

WCH-GS, 1998

Mediators of Shock and Sepsis (1)

1) Endotoxincell wall component of gram-negative bacteriapotent mediator in the development of septic shockthe host response to endotoxin

- activation of macrophages, complement and coagulation system

- release of numerous mediators: TNF-α, IL-1, IL-6, PAF, nitric oxide and various oxidants.

WCH-GS, 1998

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2) Complement Fragmentsactivation of complement descade : C5a, C3aHost response (1) release of histamine (2) vasodilatation, chemoattractincreased vascular permeability

WCH-GS, 1998



3) Eicosanoids

WCH-GS, 1998

Balance between PGI2(prostacyclin) and Thromboxane A2

” mal-distribution of blood flow”

PGE2

Leukotrienesleukotriene B4

leukotrienes C4 and D4

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Function of Eicosanoids

WCH-GS, 1998

Counteraction


4) Kininsbradykinin and kallidin(lysyl bradykinin) are low

molecular-weight peptides① development of inflammation, anaphylaxis, and septic

shock② vasodilatation, increase in capillary permeability, and

local edema formation③ pain at local wound site④ activate phospholipase formation of eicosanoids

further amplification of inflammatory response.

5) Nitric oxideendothelium derived relaxing factor

WCH-GS, 1998

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6-1) Cytokinescytokines = “small peptide molecules”direct and indirect interaction with various cell

WCH-GS, 1998

Cytokine Effects Secretary cellsInterleukinsIL – 1 Stimulates release of TNF-α, IL-6, IL-8, platelet

activating factor, prostaglandinsStimulates T and B cellsCauses feverPromotes acute-phase protein production and release

monocytes,tissue macrophage,endothelial cells,neutrophils,B lymphocytes,

IL – 2 Stimulates release of TNF-α and IFN-γCauses hypotensionEnhances T-cell proliferation and cytotoxic T- cellfunction

T lymphocytes

IL – 6 Stimulates acute-phase protein production andrelease

Cause feverEnhances neutrophil activation and accumulation

monocytes,macrophages,fibroblasts,neutophils


6-2) Cytokines

WCH-GS, 1998

Tumor Necrosis FactorTNF – α

“Principlemediator insepsis”

Stimulates release of IL - 1, IL - 6, platelet activatingfactor, prostaglandins

Promotes activation of neutrophils, eosinophils,monocytes

Activates complement and coagulation cascadesIncreases vascular permeabilityCauses hypotensionCauses fever

monocytes,macrophages,lymphocytes,Kupffer cells, andother cell types

Colony Stimulating FactorsGCSF Stimulates growth of granulocytesGM-CSF Stimulates growth of granulocytes, eosinophils, and

macrophagesInterfernsIFN-γ Stimulates release of TNF-α, IL-1, IL-6

Promotes macrophage activation and functionT cellsmacrophage populations

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7) Platelet activating factoramplify TNF-α and IL-1.

8) Endogenous opioidsenkephalins and beta-endorphins

9) Oxidantsreactive oxygen metabolitessuperoxide anion(O2ㆍ ) , hydrogen peroxide(H2O2), hydroxyl radical(OHㆍ)Ischemia-reperfusion injury

- activated neutrophilsDeleterious effects of oxidants : multiple

WCH-GS, 1998


WCH-GS, 1998

10) Neuroendocrine mediators; injury, stress, infection catabolic or stress

hormones(catechols, cortisol, and glucagon).catechols(epinephrine and norepinephrine)

- tachycardia, inotropy, peripheral vasoconstriction, increased metabolic rate,increased glycogenolysis / gluconeogenesis, and inhibition of insulin secretion

cortisol - proteolysis, lipolysis and gluconeogenesisglucagon - gluconeogenesis and glucose intolerancerenin-angiotensin system

- angiotensin II further vasoconstriction ischemia/shock

- aldosterone and vasopressin : salt and water retention

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Diagnosis and Management of Shock : General approach(1)

“the ultimate goals in the management of shock are to restore perfusion and adequate oxygen delivery to tissue.”

WCH-GS, 1998

Three parameters

1. SaO2 > 90%2. Hb. conc. > 10- 13 g/L3. Adequate cardiac output

Hypovolemic shock (1) - Definition

Loss of body fluid intravascular volume depletionpoor function of compensatory mechanisms

Types) according to the type of fluid loss a) whole blood loss --- hemorrhagic shock after traumab) plasma or free water loss

--- extracellular fluid sequestration, inadequately replaced gastrointestinal fluid loss, orexcessive insensible fluid loss : burn, pancreatitis,

or intestinal obstruction.

WCH-GS, 1998

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Hypovolemic shock (2) - Clinical signs and Symptoms

“according to the severity of fluid loss”

WCH-GS, 1998

Percent Lossof CirculatingBlood Volume(Volume Loss

for 70-kg.Male)

PulseRate

SystolicPressure

PulsePressure

CapillaryRefill Respirations

CentralNervousSystem

UrineOutput

<15%(<750ml.)

Normal Normal Normal Normal Normal Normal Normal

15%-30%(750-1500ml.)

>100 Normal Decreased Delayed Mildtachypnea

Anxious 20-30ml./hr.

30%-40%(1500-2000ml)

>120Weak

Decreased Decreased Delayed Markedtachypnea

Confused 20ml./hr.

>40%(>2000ml.)

>140Nonpalpable

MarkedDecrease

Markeddecrease

Absent Markedtachypnea

Lethargic Negligible

Ist sign of hypovolemic shock = decreased pulse pressure

Hypovolemic shock (3) - Compensatory mechanism

WCH-GS, 1998

“ to restore homeostasis and preserve blood flow to vital organ”

a) increased sympathetic output b) ADH, Renin-angiotensin system, Aldosterone

Antidiuretic hormone(ADH)increase water reabsorption in the distal tubule(kidney)

Renin- angiotensin systemangiotensin II : powerful vasoconstrictorrelease aldosterone from the adrenal cortex

AldosteroneNa+ reabsorption on renal tubule volume expansion

c) microcirculatory autoregulation↓ capillary hydrostatic pressure↑ intravascular osmolarity intravascular shift of fluid

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Hypovolemic shock (4) - Compensatory mechanism

WCH-GS, 1998

Hypovolemic shock (5) - Diagnosis

History and physical examinationCBC : change of Hct. !!

Hemodynamic monitoring- low right and left sided filling pressures

(low CVP and low PCWP)- decreased cardiac output, decreased Svo2- increased systemic vascular resistance

Symptom and signs of hypovolemic shock- signs of adrenergic discharge to the skin- oliguria- hypotension and electrocardiographic signs of myocardial

ischemia- neurologic signs and symptoms

WCH-GS, 1998

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Hypovolemic shock (6) -Treatment

A. Initial Resuscitation Phase1. airway and ventilation and oxygenation2. bleeding control3. I.V. Line 4. fluid resuscitation ;

a) isotonic electrolyte solution(such as Ringer's lactate)- rapid infusion 1-2 L/hr- refractory hypotension after infusion continuous

blood lossb) blood transfusion

- fully cross-matched blood

※ Paradox of fluid resuscitation

WCH-GS, 1998


WCH-GS, 1998

B. Monitoring of resuscitation- central venous pressure, pulmonary artery catheter monitoring

- urinary output to a rate of 0.5 to 1.0ml/kg/hour - normal heart rate and blood pressure- adequate capillary refill - normal sensorium

C. Sequestration phase management- maintain fluid resuscitation for 1 day- until diuretic phase

D. Diuretic phase- normal body fluid compartment

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WCH-GS, 1998

E. Adjunctive measure(1) pneumatic anti-shock garment(PASG)

- currently, only indication = pelvic fracture(2) colloid solutions and hypertonic saline solutions

- colloid solutions : albumin, fresh frozen plasma,dextran, hetastarch

- hypertonic solutions : 3% NaCl or 7.5% NaCl - theoretical advantage of hypertonic solution- does not use routinely

3) blood substitutes ; used in clinical study base- perfluorocarbon-based solutions- various stroma-free hemoglobin solutions

Traumatic Shock

WCH-GS, 1998

Characteristics (vs. hypovolemic shock)

(1) larger volume losses(2) greater fluid sequestration in the extravascular

compartments(3) intense activation of inflammatory mediators and

development of SIRS의차이점을가지는데

poorly response to initial fluid replacement therapyneed more intensive managementcommon Multiple Organ Dysfunction / Failure

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Common causes of compressive cardiologic shock related with hypovolemic shock

WCH-GS, 1998

Cardiogenic Shock

Causes Diagnosis TreatmentTensionpneumothorax

Profound hypotension, absence of breathsound and hyperresponance on the affectedside, distended neck vein, trachea deviation tothe opposite side

Inserting needle into the chest (2nd or 3td intercostal space)thorachotomy tube

Pericardialtanponade

After penetrating injury of chestBeck’s triad; hypotension, distended neckvein, muffled heart sound/ pulsus padoxusEchocardiography : most sensitive method

PericardiocentesisOr subxiphoid pericardiotomy

Use of Vasopressor(1)

; dopamine, dobutamin, epinephrine, norepinephrine, isoproterenol

WCH-GS, 1998

Drugs Receptors Action modeEpinephrine α1, α2, β1, β2 At low dose : β predominant

At high dose : α predominant ,marked pulse pressure, increased HR

Norepinephrine α1, α2, β1 Slightly increased pulse pressure, down HRPhenyephrine α1> α2 VasoconstrictionIsoprotenol β1 = β2 Increased HR,Dobutamine β1 > β2 Inotropic, vasodiltation, less tachycardiaDopamine Dopamine < 5 µg/kg/min : dopaminergic

(renal/splanchnic vasodilatation)5~ 15 µg/kg/min : β1 agonist (inotropic)>15~20 µg/kg/min : α agonist (vasoconstriction)

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Use of Vasopressor(2)

WCH-GS, 1998

“ Case by Case “

Neurogenic Shock

Cause ) severe head injury, spinal cord injury,pharmacologic sympathetic blockade

(high spinal anesthesia)mechanism ) sympathetic denervation

impairment of vasomotor tonesign and symptom )

- hypotension and bradycardia --- classic sign- extremities : warm and dry

treatment )- improve cardiac filling by intravenous volume

administration- Trendelenburg position- α-adrenergic agonist agents(phenylephrine) : rarely

WCH-GS, 1998

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Anaphylactic and Anaphylactoid shock(1)

Anaphylaxis : allergic response mediated by IgE antibody.antigens - insect venom, drugs, and certain foods.

Anaphylactoid reaction : not immunologically mediated.intravenous radiographic contrast dyes, narcotics in high doses,various colloids(dextrans and hydroxyethyl starch)

Mechanism )- activation and release of inflammatory mediators

(anaphylatoxins C3a and C5a, histamine, kinins, prostaglandins and others)

- vasodilatation, increased capillary permeability, bronchospasm, airway edema, circulatory collapse secondary to a sudden decrease in systemic vascular resistance and a fall in cardiac output.

WCH-GS, 1998

Anaphylactic and Anaphylactoid shock(2)

Management )- adequate airway / oxygen supply / epinephrine injection.

0.3 to 0.5 ml of epinephrine in a 1:1000 dilution/SQintravenous continuos infusion, rate of 0.5 to 5㎍/minintravenous bolus injection, 0.1 to 0.2 ml. of a 1:1000 solution.

- prevent bronchospasminhaled nebulized solutions of metaproterenol or albuterolaminophylline(5-6 mg./kg. load, followed by 0.3-0.9 mg./kg./hour)corticosteroids(250mg. hydrocortisone intravenous every 6 hours)antihistamine(25-50mg. hydroxyzine or diphenhydramine IM)

WCH-GS, 1998

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Hypoadrenal shock

Must rule out hypoadrenal shock if (1) history of glucocorticoid therapy

(2) refractory to fluid and pressure resuscitation

Diagnosis )Addison’s disease without hyperpigmentation / weight

loss / G-I symptomsLab. : Hypoglycemia with hypotension,

hyponatremia, hyperkalemiaRapid ACTH stimulation test

(250 µg of ACTH, single dose, 30 min-60 min) Treatment ) steroid replacement and hydration

Dexamethasone 4 mg (Glucocorticoid replacement)Hydrocortisone 100 mg (mineralcorticoid replacement)

WCH-GS, 1998

Shock associated with SIRS, Sepsis and MOD

Background)

Systemic inflammatory mediator With infection versus Without infection

WCH-GS, 1998

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SIRS, Sepsis and MODS(1) - definition

WCH-GS, 1998

Systemic inflammatoryresponse syndrome(SIRS)

2 or more indications1) B.T.>38°C or <36°C2) H.R> 90 /min3) R.R> 20 /min or

PaCO2 < 32 mmHg4) WBC > 12,000 or

WBC < 4,000 orBand form > 10%

26% of SIRS Sepsis

7% of SIRS septic shock

Mortality= 7%

Sepsis SameCultureproveninfection

Mortality=16%

Septic shock Same same

Hypotensiondespite TxWithhypoperfusion(acidosis/oliguria/acute alteration ofmental status)

Mortality=46%

Multiple organdysfunction syndrome(MODS)

Presence of altered organ function in acutely ill patientHomeostasis cannot be maintained without intervention

Mortality=20-100%

SIRS, Sepsis and MODS(2) – Significance

Clinical continuum of SIRD/ Sepsis/ MODS possible

(1) Early diagnosis and Treatment (2) Development of pre-hospital or primary care unit

management(3) Risk factor analysis

WCH-GS, 1998

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SIRS, Sepsis and MODS(3) - Development of MODS

“ Two hit theory of the development of MODS”

WCH-GS, 1998

PrimaryMODS

Early and direct result of insultex) thoracic trauma- pul. Contusion rhabdomyolysis – renal failureFig

SecondaryMODS

Amplified systemic inflammatoryresponse late and remote organ dysfunction“vicious cycle”

SIRS, Sepsis and MODS(4) - Clinical Features

WCH-GS, 1998

Stage Hemodynamic profile Clinical Sx and Lab.

Earlystage

Hyperdynamic1. increased cardiac output2. decreased peripheral vascular

resistance3. vascular volume is expanded4. vasodilation5. underperfused splanchnic circulation

1. Warm skin2. hypermetabolism ; increased in resting

energy expenditure/ gluconeogenesis/catabolism/ oxygen consumption

Latestage

Hypodynamic1. low cardiac index2. tachycardia3. hypotension4. decreased or increased peripheral

vascular resistance

1. fever or hypothermia2. oliguria3. deterioration of mental status4. leukocytosis or leukocytopenia

“ high mortality and morbidity”

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SIRS, Sepsis and MODS(5) – Cause of sepsis

Infectious Site )pneumonia, gastrointestinal perforation, biliary tract infection, urinary tract infection, burn, line sepsis from indwelling intravenous catheter

Organism ) Gram negative – E.coli, Klebsiella, Pseudomonas,

Bacteroides Gram positive – Staphylococcus, StreptococcusOthers – fungus, virus, protozoa : less common

WCH-GS, 1998

SIRS, Sepsis and MODS(6) – Score of MOD

MODS(dysfunction syndrome) = “The Clinical Syndrome”

Organ failure versus Organ DysfunctionAl l or none versus Score system

WCH-GS, 1998

Organ Grade 1 Grade 2 Grade 3Kidney Scr > 1.0 mg% Scr > 2.5 mg% Scr > 5.0 mg%Liver Bilirubin > 2.0 mg% Bilirubin > 4.0 mg% Bilirubin > 8.0 mg%Heart Minimal inotropic support

< 5µg/kg/minModerate inotropic support5-15 µg/kg/min

High inotropic support> 15µg/kg/min

Cardiac index < 2.2 L/min/M2 requiring inotropic supportLungs ARDS score > 5 ARDS score > 9 ARDS score > 13ARDS score = a. Chest PA + b.PaO2/FiO2 + c.Minute ventilation + d. Positive end-expiratorypressure + e. Static compliance

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SIRS, Sepsis and MODS(7) – Risk factors

Factors affecting to the MODS. pre-existing disease . advanced age. nature and intensity of inciting event/second hit. presence of sepsis

Factors affecting to the patient survival rate. numbers of involved organ. type and combination of involved organs

WCH-GS, 1998

(1) Pulmonary dysfunctionappears at early stagepathophysiology : capillary endothelial injury,

interstitial edema, ischemic alveolar injuryclinical consequence : ARDS (V-P abnormality,

pulmonary edema, refractory hypoxia)treatment : ventilatory careprognosis : mortality > 50%

(2) Gastrointestinal dysfunctionclinical course : gastritis, ulceration, ileus,

pancreatitis, acalculous cholecystitispathophysiology : breakdown of gut mucosa barrier

bacterial translocation sepsis

WCH-GS, 1998

(1) Pulmonary dysfunction

appears at early stage

pathophysiology : capillary endothelial injury, interstitial edema, ischemic alveolar

injury

clinical consequence : ARDS (V-P abnormality, pulmonary edema, refractory hypoxia)

treatment : ventilatory care

prognosis : mortality > 50%

(2) Gastrointestinal dysfunctionclinical course : gastritis, ulceration, ileus, pancreatitis, acalculous cholecystitispathophysiology : breakdown of gut mucosa barrier bacterial translocation sepsis

SIRS, Sepsis and MODS(8) - MODS

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(3) Liver dysfunctionLiver : vital organ for (1) metabolic function,

(2) clearing of toxin /bacteria /inflammatory mediator

clinical : increase the plasma level of glucose, triglyceride, amino acid, bilirubin, urea

role of kupper cell : critical role in detoxication of toxin

(4) Renal dysfunctionappears in early stagepathophysiology : tissue hypoperfusion or direct

tissue damage by inflammatory mediatorstreatment : avoidance of nephrotoxicity drug,

aggressive resuscitation, if need dialysisWCH-GS, 1998


(5) Cardiac dysfunctionmyocardial depression due to myocardial

depressant factorscause of myocardial depression : unclear

(6) Central nervous systemusually late onsetmeasured with Glascow coma score

WCH-GS, 1998

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SIRS, Sepsis and MODS(11) – Treatment

Best treatment = “ preventing the progression of MODS”

Goal of treatment =’ maintains the optimal level of oxygen delivery and consumption ”

- Early treatment before Organ dysfunction - Invasive monitoring system - High mortality

WCH-GS, 1998


1. broad-spectrum antibiotics, initial narrow spectrum antibiotic after culture result

2. routinely identify possible source of infection3. elimination of infection focus ex) if need, surgical

debriment and drainage4. reduction of nasocominal infection5. nutritional supply : 25-35 Kcal/kg/day of calories with 1.5

~ 2.0 gm/kg/day of protein ( positive protein balance )

WCH-GS, 1998

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Advanced pharmacologic approach : “mediator regulation”

corticosteroids NSAID(non-steroidal anti-inflammatory drug)various antioxidantsantiendotoxin antibody IL-1 receptor antagonistmonoclonal antibodies against tumor necrosis factorplatelet activating factor receptor antagonistmacrophage-specific immunomodulators

WCH-GS, 1998

Definition of shockPathophysiology of shock – hypoxia, anaerobic metabolism,

acidosis, circulation redistributionMediator of shock – Eicosanoids, cytokine, oxidantsGeneral principles of shock management – O2, Hb, COHypovolemic shock

- compensation mechanism- early management- monitoring of resuscitation

Traumatic shock, Cardiogenic shock, Neurologic shockSIRS, Sepsis, Septic shock, MODS

- definition- clinical progress and multiorgan failure- Treatment

Summary

Documents

Myoung Soo Kim M.D. - gs.yonsei.ac.krgs.yonsei.ac.kr/download/Slide_shock_2003.pdf6 Pathophysiology of shock (4) C. Circulatory redistribution “For preservation of vital organ”