Shock Corrected

8/6/2019 Shock Corrected

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IntroductionTypes and causes of shock

Pathophysiology of shockStages and clinical features of shockFirst stage or non-progressive shockSecond stage or progressive shockThird stage or refractory shockTreatment of shock with physiological basis

Applied


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DefinitionIn 1852, shock was defined as a rudeunhinging of the machinery of life.

Shock is a clinical syndrome characterized byinadequate tissue perfusion due to low cardiacoutput ( or acute circulatory failure).

The cardinal features of all type of shock is lowcardiac activity.


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FIR ST STAGE OR NON

PR G OR ESS IV E SH OCK A non p r og r essive st a ge(co m pens a te d st a ge ).

o Compensa ted shock o Modera te reduc t ion in CO

o Compensa tory mechanism-


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R A PID COMP E NSAT ORY

ME CHA N I S M (N EU R AL ME CHA N I S M)BA R OR E CE PT OR R E F LEX -

H emorrhage (Blood loss)

D ecrease Blood Volume

D ecrease V enous Pressure

D ecrease V enous R eturn

D ecrease At rial Pressure

D ecrease V en tricular end-dias tolic volume

Cardiac MuscleD ecrease St roke V olume

D ecrease Cardiac Ou t pu t

D ecrease A r terial Blood pressure


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CHEMORECEPTOR REFLEX

Acute hemorrhage loss of RBCs and reduce O2

carrying capacity anemia &stagnant hypoxia ,

acidosis stimulate chemoreceptors excite

vasomotor centre.Fall in BP below 60mmhg usually initiates

chemoreceptor reflex.


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CNS ISCHEMIC RESPONSE

Fall in BP


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INTERMEDIATE COMPENSATORY

MECHANISM

1. Renin angiotensin vasoconstrictory mechanism.

2. Reverse stress relaxation.

3. Capillary fluid shift mechanism


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RENIN-ANGIOTENSIN-ALDOSTERONE

D ecrease in plasma volume / decrease in Na +

Detected by

Kidney (Jux traglomerular appara tus) Release

R enin

ConvertsA ngo tensin I

Via ACE


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A ngio tensin II

A drenal Cor texR eleases

A ldos terone

Increase S odiumR eabsorp t ion

Increase fluidvolume

Increase BP

IncreaseV asocons tric t ion

PVR

Increase BP

Increase T hirs t

Increase fluidvolume

Increase BP

Increase A D H (A nti D iure t ic

hormone)

Increase fluid

volume

Increase BP


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REVERSE STRESS RELAXATION

MECHANISMProlong slow

bleeding

R everse s tressrelaxa t ion

mechanism

Correc t up to 15%change in blood

volume below normal

D ecrease BPT igh tening of vessel wall

by vascular toneadjus tmen t secondary toless s tress on vessel wall

R es tore BP back tonormal


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CAPILLARY FLUID SHIFT MECHANISM

D ecrease BP

Mean capillary pressure islow

A bsorp t ion of fluid fromin ters t ial fluid compar tmen t

to circula

tion

T hus,blood vol. increasedres tore BP normal


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LONG TERM COMPENSATORY MECHANISM

1. Restoration of plasma volume and protein

2. Restoration of red cell mass


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RESTORATION OF PLASMA VOLUME

AND PROTEIN- After moderate hemorrhage the plasmavolume is restored n in 12-72 hrs bez of increase in plasma water along withelectrolyte content.Hemodilution occursRapid entry of preformed albumin fromextravascular storesPlasma protein loss is restored byhepatic synthesis over a period of 3-4days.


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Restoration of red cell mass

Excessive release of erythropoietin which

the rate of cell production in the bone

marrow within 10 days.


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PROGRESSIVE SHOCK

Occurs after 15-25% loss of total blood volume.

In this stage compensatory mechanisms are not

able to stop the progression of shock.

Intense arteriolar vasoconstriction is inadequate for

maintenance of normal BP.Various Positive Feedback mechanism develop.


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EFFECT ON BODY TISSUE IN

PROGRESSIVE SHOCK W idespread cellular degeneration (liver,lung&heart).active transport of Na and K through cell membraneresulting in accumulation of sodium in the cells and loss of

K from the cell so cell begins to swellMitochondrial activity in liver cells &other cellsMetabolism of glucose is depressed in last stages of shock.Poor delivery of O2 to tissue oxidative metabolism thecells switch to anaerobic glycolysis of lactic acid in theblood

Accumulation of CO2 leading to Acidosisvasodilatation aggravates shock vicious cycle starts


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REFRACTORY SHOCK

In this stage all the therapeutic interventions areusually ineffective and eventually the patient dies.

Causes of refractiveness of shock-Depletion of high energy phosphate compoundsSlow necrosis of cells esp near venous end of capillary, patchy necrosis first appears in cells of

liver, kidney tubules ,lungs ,heart .Kidney acute tubular necrosis acute renalfailure uraemic death.Deterioration of the lungs respiratory distress

shock lung syndrome.


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Khurana book of human physiology


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TYPES OF SHOCK

1. Hypovolaemic shock

2. Low-resist or distributive or vasogenic shock

3. Cardiogenic shock

4. Obstructive shock


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HYPOVOLEMIC SHOCK Hypovolemia means diminished blood

volume

Haemorrhage is the most common cause

Cardiac output and arterial pressure falls to

Zero when 35-45 % of total blood volume

removed.


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CAUSESHemorrhagic

G I BleedT raumaMassive hemop tysisPos t par tum bleeding

N on hemorrhagicV

omiting

D iarrhoeaBowel obs truc t ion/ Pancrea t it isBurns


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CLINICAL FEATURESH ypo tensionT achycardiaR apid shallow brea thingCold, pale, clammy skinI ntense thirs t


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H ypovolemic shock is fur ther subdivided infollowing ca tegories on basis of causes.

H emorrhagicT rauma t icS urgicalD

ehydration shock

Mos t common type is hemorrhagic shock


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HEMORRHAGIC SHOCK I f the blood loss is up to 10-30%compensa tory changes take place and normal

condi t ion is res tore.I f the blood loss is severe up to 40% of bloodvolume then condi t ion progresses leading to

circulatory collapse and dea

th.


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Ctd.

MECHANISM OF DEVELOPMENT OF SHOCK:

H a e m o rr h a ge

Ci r cu la ting bl oo d vo lu m e

Tissue pe r fusion

A n a e r o b ic g ly co ly sis

La ctic- a ci d osis

i) Dep r esses the my oc ard iu mii ) Dec r e a ses pe r iphe ral v a scu lar r esponsiveness to

c a techo lam ines,

Co ma


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HYPOVOLEMIC SHOCK


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APPROACH TO PATIENT OF

HYPOVOLEMIC SHOCK Hypotension / Tachycardia

A irway con trol

A ssure ven t ila t ionA ugmen t circula t ion(Crys talloid Blood)

V S uns table

(H ear t ra te > 120and / or S BP 15Consider

Cardiac dysfunc t ionT amponade

T rea t appropria tely


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V ital sign uns tableor acidosis worsen

I nser t PA C

Cardiac I ndex


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D is tribu t ive or vasogenic shock T here is no loss of blood ins tead there is increase invascular capaci ty.

T his is due to decrease in vascular tone.T hree types- a) Neurogenic shock.

b) A naphylac t ic shock.c) S ep t ic shock.


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CausesS pinal anes thesia.D irec t damage to vasomo tor cen tre of themedulla.A ltered func t ion of the vasomo tor cen tre inresponse to low blood glucose level (insulin

shock)


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T ypesV asovagal syncope.Pos tural syncope.

Mic tura t ion syncope.Caro t id sinus syncope.Cough syncope.


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MechanismD ecrease symp tha t ic tone or increase parasymp tha t ic tone

D ecrease vascular tone

Massive vasodila tat ion

Decrease

S VR and preload

D ecrease cardiac ou t pu t

D ecrease t issue perfusion


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T rea tmen tF luid resusci tat ion

- to keep M A P a t 85-90 mmhg for firs t 7days.

- if crys talloid are insufficen t vasopressorscan be used.

- Bradycardia At ropine

- pacemaker - me thyl prednisolone mus t be s tar ted wi thin 8hrs.


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A NA PH Y LA CT I C SH OCK A NA PH Y LAX I S - a severe sys tema t ichypersensi t ivi ty reac t ion charac terized bymul t isys tem involvemen t .I t is I gE media ted.

A NA PH Y LA CT OID R EA CT I ON- clinicallyindis t iquishable from anaphylaxis.D o no t require sensi t izing exposure.

No t I gE media ted.


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MechanismA cu te allergic reac t ion

L arge quan t ity of his tamine like subs tance released

Mark vasodila tat ion

R educed peripheral resis

tance

I ncrease in capillary permeabili ty

F luid loss and hypovolemia


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S ymp tomsPruri t is , flushing , ur t icaria.T hroa t fullness.A nxie tyChes t t igh tnessS hor tness of brea thA ltered men tal s tatus.R espira tory dis tress.


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Mild localized ur t icaria can progress to fa tal

anaphylaxis.S ymp toms usually begin wi thin 60 sec of exposure.F as ter the onse t of symp toms = more severe isreac t ion.

BI PHAS I C P HE NOM A NON- occurs in sever anaphylaxis.

a) symp toms re turn 3-4 hrs af ter ini t ial reac t ion hascleared.

40- 60% for insec t st ings20- 40 % for radio con tras t agen t .

10-20 % for drug.


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T rea tmen t E pinephrine 0.3mg I M of 1:1000

- repea t every 5 -10 mins as

needed.-cau t ion wi th pa t ien ts on be ta

blocker ( causes severe hyper tension due to

unopposed alpha s t imula t ion.)- if refrac tory s tar t IV drip 2-8

ugm min.


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Cor t icos teroidsa) prednisolone 50 mg od

b) Me thylprednisolone 125 mg IV odA nt ihis taminic

a) H 1 blocker diphenhydramine b) H 2 blocker rani t idine.

Bronchodila tors albu terol .G lucagon for p t taking be ta blocker and wi threfrac tory hypo tension.

1 mg IV in 5 divided doses.


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SE PT I C SH OCK Bactremia: Presence of bacteria in blood, asevidenced by positive blood cultures.

Septicemia: Presence of microbes & their toxins in

blood

SIRS: Two or more of the following conditions:1) Fever (oral temperature >38 0C) or Hypothermia

(24 breaths/min),

3) Tachycardia (heart rate >90 beats/min),4) Leukocytosis (>12,000/l), or >10% band forms orLeukopenia (


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Severe sepsis: Sepsis with one or more signs of organ dysfunction

Septic shock: Sepsis with hypotension arterial blood pressure 1 h and

does not respond to fluid or pressor administration

MODS: Dysfunction of more than one organ requiring intervention to maintain homeostasis.


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ET IO

LO

G Y


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CA RDI

OGE

NIC

SHOCK

D E FI NE D AS -A ) S BP < 90 mmhg.

B) C I < 2.2 l/m2.C) PCWP > 18 mmhg.


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Decrease pumping ability of the heart because of cardiac abnormality.Severe depression of the systolic cardiacperformance is key factor in causing this type of shock.Inadequate pumping of venous return congestionof lung and viscera (congested shock).


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S igns cool mo tt led skin- tachypnoea

- hypo tension- A ltered men tal s tatus

- narrowed pulse pressure


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S ystolic BPdefines 2 nd line of

action

NTG if S BP > 100mmhg

D opamine if S BP70-100

D obu tamine if S BP < 100

S BP > 100 S BP 70-100no signs of

shock

S BP 70-100signs of shock

S BP < 70sings of shock

NTG 10-20 mug /

min

D obu tamine 2 to 20mug kg /

min

D opamine 2-20

mug/kg/min

Norepineprine 0.5 to 30

mug/min

Iden t ify & trea t reversible causes

PA CI A BP

A ngiography & PC I


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I ntra aor t ic balloon pump ( I A BP)

- A ugmen ts coronary blood flow in dias tole.- Balloon collapse in sys tole crea tes a vacuum

effec t .---- decrease af terload.- D ecrease myocardial o2 demand.


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Contraindica

tion

S ignifican t A R A bdominal aor t ic aneurysmU ncon trolled sepsisU ncon trolled bleeding disorder Peripheral vascular disease


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Complication

Cerebro vascular episodeS epsis

Ballon rup tureT hrombocy topeniaPeripheral neuropa thy


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OBSTRUCTIVE SHOCK

Impairment of ventricular filling during diastoledue to external pressure on heart.ventricular filling & stroke volume cardiacoutput circulatory shock.causes

1. Peripheral cardiac temponade2. Tension pneumathorax

3. Constrictive pericarditis4. Pulmonary embolism


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Di i h h k


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MI, PTE,

Tension Pneumothorax,

Cardiac Tamponade, Sepsis

Sepsis Sepsis, Anaphylaxis

Hemorrhage Na/H 2Oloss

Diagnostic approach to shock

Documents

Shock Corrected