Haemorrhagic Haemorrhagic shockshock

A presentationA presentation

Definition-Shock is the clinical Definition-Shock is the clinical syndrome that results from syndrome that results from

inadequate tissue perfusion which inadequate tissue perfusion which leads to hypoxia and ultimately leads to hypoxia and ultimately cellular dysfunction.The cellular cellular dysfunction.The cellular

dysfunction is manifested as lactic dysfunction is manifested as lactic acidosisacidosis..

ETIOLOGYETIOLOGY

Causes of haemorrhagic shock-Causes of haemorrhagic shock-ectopic pregnancy,acute operative ectopic pregnancy,acute operative

loss,trauma,retroperitoneal loss,trauma,retroperitoneal bleed,obstretic haemorrhage like bleed,obstretic haemorrhage like

antepartum haemorrhage,post antepartum haemorrhage,post operatively-primary and secondary operatively-primary and secondary

hemorrhagehemorrhage

Body Fluid CompartmentsBody Fluid Compartments

Approximately two thirds of the body Approximately two thirds of the body water is intracellular and the water is intracellular and the remaining one third is in the remaining one third is in the

extracellular compartment which is extracellular compartment which is distributed between the interstitial distributed between the interstitial

compartment and intravascular compartment and intravascular compartments in a 3:1 ratiocompartments in a 3:1 ratio

Compensatory mechanisms in Compensatory mechanisms in shockshock

11..plasma refillplasma refill 22..RAS and the hypothalamic hypophyseal RAS and the hypothalamic hypophyseal

adrenal system -Renin converts adrenal system -Renin converts angiotensinogen to angiotensin1 which is angiotensinogen to angiotensin1 which is metabolised in the liver to angiotensin2,a metabolised in the liver to angiotensin2,a

potent vasoconstrictor that stimulates potent vasoconstrictor that stimulates aldosterone secretion,along with the aldosterone secretion,along with the

pituitary release of ADH,promoting sodium pituitary release of ADH,promoting sodium and water retentionand water retention . .

Compensatory mechanisms in Compensatory mechanisms in shockshock

33..Norepinephrine and epinephrine are Norepinephrine and epinephrine are locally and systemically locally and systemically

released.Catecholamine mediated effects released.Catecholamine mediated effects are inotropic and chronotropic resulting in are inotropic and chronotropic resulting in

increased cardiac output.They also increase increased cardiac output.They also increase the systemic vascular resistance leading to the systemic vascular resistance leading to

incresed diastolic pressure and therefore incresed diastolic pressure and therefore narrow pulse pressurenarrow pulse pressure..

44..Venoconstriction enhances venous return Venoconstriction enhances venous return which also increases cardiac output and which also increases cardiac output and

stroke volumestroke volume..

Phases of shockPhases of shock

EARLY SHOCK-The compensatory EARLY SHOCK-The compensatory mechanisms are intact and the shock is mechanisms are intact and the shock is

almost eventually reversiblealmost eventually reversible..

INTERMEDIATE SHOCK-Compicated shock INTERMEDIATE SHOCK-Compicated shock associated with loss of compensatory associated with loss of compensatory

mechanismsmechanisms..LATE OR COLD SHOCK-shock is irreversible LATE OR COLD SHOCK-shock is irreversible

since cellular injury has occurred to the since cellular injury has occurred to the heart and brainheart and brain..

Haemorrhagic shockHaemorrhagic shockClass 1Class 1Class 2Class 2Class 3Class 3Class 4Class 4

Blood loss (in Blood loss (in ml)ml)

<<750750 mlml 750-1500750-15001500-20001500-2000>>20002000

Blood Blood volume (in%)volume (in%)

<<151515-3015-3030-4030-40>>4040

Heart rateHeart rate<<100100>>100100>>120120>>140140

Blood Blood pressurepressure

Normal or Normal or increasedincreased

Normal Normal (+tilt )(+tilt )

Decreased Decreased mean arterial mean arterial pressure<60pressure<60

decreaseddecreased

Pulse Pulse pressurepressure

NormalNormal DecreasedDecreased

DecreaseDecrease

decreaseddecreased

Capillary Capillary refillrefill

NormalNormal May be May be delayeddelayed

Usually Usually delayeddelayed

Always Always delayeddelayed

RespirationsRespirations

normalnormalMildly Mildly delayeddelayed

Usually Usually delayeddelayed

Always Always delayeddelayed

Urinary Urinary output output (ml/hr)(ml/hr)

> > 303020-3020-305-155-15Essentially Essentially anuricanuric

Mental Mental statusstatus

Normal or Normal or anxiousanxious

AnxiousAnxious confusedconfusedLethargic,obtLethargic,obtundedunded

HEMRRHAGIC SHOCKHEMRRHAGIC SHOCK

HYPOVOLEMIA LEADS TO HYPOVOLEMIA LEADS TO DECREASED PRELOAD WHICH LEADS DECREASED PRELOAD WHICH LEADS

TO INCREASED SYMPATHETIC TO INCREASED SYMPATHETIC ACTIVITY AND VASOCONSTRICTIONACTIVITY AND VASOCONSTRICTION

Haemorrhagic shockHaemorrhagic shock

Vasoconstriction leads to decreased Vasoconstriction leads to decreased mean arterial pressure and ischemia mean arterial pressure and ischemia

which ultimately leads to which ultimately leads to multiorgan failure-ARDS,HEPATIC multiorgan failure-ARDS,HEPATIC

FAILURE,STRESS,GI BLEEDING.RENAL FAILURE,STRESS,GI BLEEDING.RENAL FAILURE .Ischemia leads to FAILURE .Ischemia leads to

myocardial insufficiency and severe myocardial insufficiency and severe decrease in SVR and finally deathdecrease in SVR and finally death

Haemorrhagic shock (Early)Haemorrhagic shock (Early)Organ systemOrgan systemSymptom or signSymptom or signcausecause

Central nervous Central nervous systemsystem

Mental status changesMental status changesDecresed cerebral perfusionDecresed cerebral perfusion

Heart(circulatory)Heart(circulatory)Tachycardia,rapid Tachycardia,rapid thready pulsethready pulse

Adrenergic stimulation Adrenergic stimulation increases cardiac output and increases cardiac output and

SVR.Cardiac output decreases SVR.Cardiac output decreases with depressed with depressed

contractility ,decreasing SVRcontractility ,decreasing SVR

SystemicSystemicNormotensive or Normotensive or hypotensive,decreased hypotensive,decreased JVD,narrow pulse JVD,narrow pulse

pressurepressure

Decreased SVR and venous Decreased SVR and venous return secondary to volume return secondary to volume

loss.sympathetic stimulation loss.sympathetic stimulation increases vascular toneincreases vascular tone . .

RenalRenal oliguriaoliguriaDecreased perfusion due t o Decreased perfusion due t o decreased volumedecreased volume

RespiratoryRespiratory Tachypneic or normalTachypneic or normalSympathetic stimulation or Sympathetic stimulation or acidosisacidosis

SkinSkin Cold ,clammyCold ,clammyVasoconstriction ,sympathetic Vasoconstriction ,sympathetic stimulationstimulation1111

[[Priorities in management:restore Priorities in management:restore ORDERORDER]]

O:oxygenate 6-8 litres of oxygenO:oxygenate 6-8 litres of oxygen R:restore circulatory volumeR:restore circulatory volume D:Drug therapy(pharmacologic support)D:Drug therapy(pharmacologic support) E:evaluate response to therapyE:evaluate response to therapy Remedy the underlying causeRemedy the underlying cause

Signs of late shockSigns of late shock

Organ systemOrgan systemSign or Sign or symptomsymptom

causecause

CNSCNS DisorientationDisorientation,o-btundation,o-btundation

Hypoxia,worsHypoxia,worsening ening

cerebral cerebral ischemiaischemia

HeartHeart Cardiac Cardiac dysfunction,tadysfunction,tachycardia chycardia

and other and other arrythmiasarrythmias

Irreversible Irreversible ischemia,decrischemia,decreased cardiac eased cardiac index,decreasindex,decreas

ed ejection ed ejection fractionfraction

systemicsystemicDecreased Decreased JVP JVP

normotension normotension or progressive or progressive

hypotensionhypotension

RVF,extravascRVF,extravascular poolingular pooling

RenalRenal Oliguria or Oliguria or progressing t progressing t

o anuriao anuria

ARFARF

RespiratoryRespiratory TachypneaTachypnea ARDSARDS

SkinSkin Cold and Cold and clammyclammy

VasoconstrictiVasoconstriction,sympathetion,sympatheti

c stimulationc stimulation

OtherOther Lactic Lactic acidosisacidosis

Anaerobic Anaerobic metabolismmetabolism

Guidelines to manage shockGuidelines to manage shockCARDIAC INDEXCARDIAC INDEX>>2.2L/min/m22.2L/min/m2

PULMONARYPULMONARYNormalise A-a gradient(Pao2>30mm of Hg Normalise A-a gradient(Pao2>30mm of Hg or SaO2>55%) or SaO2>55%)

Blood gasesBlood gases Maintain PaO2 80-100mm of Hg,PaCo2 30-Maintain PaO2 80-100mm of Hg,PaCo2 30-35mmof Hg,pH>7.3535mmof Hg,pH>7.35

RenalRenal Maintain urine output of Maintain urine output of 20-30ml/hr;normalise BU and nitrogen20-30ml/hr;normalise BU and nitrogen

HepaticHepatic Bilirubin<3mg/dlBilirubin<3mg/dl

Mental statusMental status Restor orientationRestor orientation

Evaluation of response to initial Evaluation of response to initial attempts at fluid resusticationattempts at fluid resustication

Rapid Rapid responseresponse

Transient Transient responseresponse

No No responseresponse

Vital signsVital signs Return to Return to normalnormal

Transient Transient improve- improve-

ment ,rement ,re

currence currence of of

decreased decreased BP or BP or

increased increased heart rateheart rate

Persistent Persistent tachycarditachycardia,hypotena,hypoten

sio-sio-n ,altered n ,altered

mental mental statusstatus

Estimated Estimated blood blood

lossloss(%)(%)

Minimal(1Minimal(10-20)0-20)

Moderate Moderate and and

ongoing(2ongoing(20-40ml)0-40ml)

Severe(>Severe(>40ml)40ml)

Need for Need for more more

crystalloidcrystalloid

LowLow HighHigh HighHigh

Blood Blood preparatiopreparatio

nn

LowLow Moderate Moderate to highto high

immediatimmediatee