shock – an overview.ppt

7/24/2019 SHOCK AN OVERVIEW.ppt

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SHOCK AN OVERVIEWSHOCK AN OVERVIEW

Definition a multifaceted syndromeleading to systemic & localized tissue

hypoperfusion, resulting in cellular

hypoxia & multiple organ dysfunction


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DESCRIPTION

1. Perfusion may be decreased with obvioussigns such as hypotension

. Perfusion may be decreased due to

maldistribution as in septic shoc! wheresystemic perfusion may appear elevated

". #igns of malperfusion may be subtle & lead tosignificant organ damage

$. Prognosis determined by degree of shoc!,duration, %o of organs affected, previousorgan dysfunction & 'enetic predisposition


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ETIOLOGICAL CLASSIFICATION

( )ypovolemic *oss of circ intravascular vol & decrease in cardiac

preload +ay be hge trauma, '- bleed, nontraumatic internal

bleed aneurysm, ectopic rupture/ or bleeding P0 %onhgeic fluid loss from '- tract vomiting,diarrhea,

fistula/, urinary losses D+/, evaporative fever,hyperthermia/ & internal fluid shifts"rdspace loss asin intestinal obstruction/

linical signs depend on volume lost & rapidity of loss +ost common form2ll forms have a component of decreased preload


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ontd

( 3bstructive

+echanical obstruction to normal cardiac

output causing decrease in systemic

perfusion

ardiac tamponade, tension pneumothorax.linical signs raised 40P, muffled heart

sounds & decreased breath sounds

massive pulmonary embolism & air embolism


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contd

( ardiogenic

aused by myocardial pump/ failure

5xtensive myocardial infarction most commoncause

6educed contractility cardiomyopathy, sepsis

induced/, 2#, +#, atrial myxoma,

dysrhythmias


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contd

( Distributive

aused by systemic vasodilatation infection,

anaphylaxis/ resulting in systemic hypotension &

inc 7 dec 3

#-6# most common cause of distributive shoc! +ost common cause of #-6# is epsis

Despite the high 3 there is cellular hypoxia

due to disruption of mitochondrial function2naphylaxis, severe liver dysfunction, neurgenic

shoc! spinal trauma/ also cause distributive

shoc!


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contd

( 5ndocrine shoc!

)ypothyroidism, hyperthyroidism with cardiac

collapse, adrenal insufficiency

2drenal insufficiency may be a contributor to

shoc! in critically ill patients. ase

unresponsive to treatment should be tested

for adrenal insufficiency.


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PATHOPHYSIOLOGY

( 6esult of shoc! decreased tissue perfusion &cellular hypoxia

( ell hypoxiacellular ischemia, alteration in a,

c2+P & formation of 386

( )ypoxia enhanced vasc permiability & dec

control on memb tpt fns

( 6eperfusion release of 386 cell

damage

( %eutrophil activation & release of

proinflammatory cyto!ines


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contd

( 8urther cell damage, third spacing,activation of coag, microcirc thrombosis,

collapse & further ischemia

( -n sepsis & #-6# initial event isinflammatory response

( +icrocirculatory collapse leads to +38


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DIAGNOSIS

( 0ital signs )6, 9P, temp, urine output,

#p3 traditional measures

( :;


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contd

( >rine output end organ response to shoc!,

1 hrs needed to measure( #p3 early indicator of hypoxia, may be

invalid in hypothermic pt

( -nvasive hemodynamic monitoring better 29P, 0P, P2,#v3, 3esophageal

doppler, 8lowtrac, lidco, picco


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RESUSCITATION END POINTS

( *actic acid production

ells with inade?uate 3 will switch to

anaerobic metabolism

lactic acid byproduct of anaerobic met elevation of lactate is measure of severity of

shoc!. *actate also elevated in liver & !idney

failure, 26D#

6ate of clearance of lactate a better mar!er

for ade?uate resuscitation


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contd

( 9ase deficit

9ase deficit is amt of base re?uired to titratewhole blood to a normal p)

5levated base deficit correlates with severityof shoc!

correction of 95 is a guide to further mgnt

( -ntra mucosal p) monitoring +esentric hypodynamic response to shoc!

'astric tonometry measures intramucosal p)& is an early indicator of gut hypoperfusion,correlates with mortality

@echnically difficult less used


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TREATMENT

6apid recognition & restoration of perfusionis !ey to preventing multi organ failure &

death. -n all forms of shoc! rapid

restoration of preload with fluids is the 1st

treatment

@reat shoc! while identifying its cause

8urther treatment depends on etiology


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contd

( )ypovol shoc!

6apid infusion of large vol of fluids thru largebore -0 cannulae, central access may be

needed incl P2/

-f cause be, then after initial " ltrs of fluids,

blood is transfused

6ecent data supports use of pac!ed cells A

88P A platelets in a 1B1B1 ratio

8actor 0--a may also be useful 6esuscitation complete only when base excess

& lactate corrected to acceptable levels

0asoconstrictors rarely needed


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contd

( 3bstructive shoc!

-dentify cause & relieve early

Pericardiocentesis, pericardiectomy for

tamponade

%eedle decompression , tube thoracostomy

for tension pneumothorax

0entilatory, cardiac support, thrombolytics &

heparin for P5


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contd

( ardiogenic shoc!

3ptimise preload with infusion of fluids

3ptimize contractility with inotropes, balancing

cardiac 3 demand

2dCust afterload to maximise 3. pts may

need vasodilation to decrease #06

Diuresis may be indicated >nderlying cardiac cause needs treatment

P2 is recommended to guide therapy


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contd

( Distributive shoc!

-n #-6# & sepsis , shoc! due to toxins7mediator

induced vasodilatation

2ggressive fluid resuscitation

Pressors after infusion of volume Dobutamine, noradr, vasopressin

*ow dose steroids if evidence of adrenal

insufficiency @reat underlying cause of #-6#


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shock – an overview.ppt

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