Haemorrhagic
shock
A presentation
Definition-Shock is the clinical
syndrome that results from
inadequate tissue perfusion which
leads to hypoxia and ultimat...
ETIOLOGY
Causes of haemorrhagic shock-ectopic
pregnancy,acute operative
loss,trauma,retroperitoneal bleed,obstretic
haemo...
Body Fluid Compartments
Approximately two thirds of the body
water is intracellular and the remaining
one third is in the...
Compensatory mechanisms in
shock
1.plasma refill
2.RAS and the hypothalamic hypophyseal
adrenal system -Renin converts
a...
Compensatory mechanisms in
shock
3.Norepinephrine and epinephrine are locally
and systemically released.Catecholamine
med...
Phases of shock
EARLY SHOCK-The compensatory mechanisms
are intact and the shock is almost eventually
reversible.
INTERM...
Haemorrhagic shock
Class 4Class 3Class 2Class 1
>20001500-2000750-1500<750 mlBlood loss (in
ml)
>4030-4015-30<15Blood volu...
HEMRRHAGIC SHOCK
HYPOVOLEMIA LEADS TO DECREASED
PRELOAD WHICH LEADS TO INCREASED
SYMPATHETIC ACTIVITY AND
VASOCONSTRICTION
Haemorrhagic shock
Vasoconstriction leads to decreased mean
arterial pressure and ischemia
which ultimately leads to mult...
Haemorrhagic shock (Early)
causeSymptom or signOrgan system
Decresed cerebral perfusionMental status changesCentral nervou...
[Priorities in management:restore
ORDER]
O:oxygenate 6-8 litres of oxygen
R:restore circulatory volume
D:Drug therapy(p...
Signs of late shock
causeSign or
symptom
Organ system
Hypoxia,worsen
ing cerebral
ischemia
Disorientation,o
-btundation
CN...
Guidelines to manage shock
>2.2L/min/m2CARDIAC INDEX
Normalise A-a gradient(Pao2>30mm of Hg or
SaO2>55%)
PULMONARY
Maintai...
Evaluation of response to initial
attempts at fluid resustication
No
response
Transient
response
Rapid
response
Persistent...
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Haemorrhagic shock

  1. 1. Haemorrhagic shock A presentation
  2. 2. Definition-Shock is the clinical syndrome that results from inadequate tissue perfusion which leads to hypoxia and ultimately cellular dysfunction.The cellular dysfunction is manifested as lactic acidosis.
  3. 3. ETIOLOGY Causes of haemorrhagic shock-ectopic pregnancy,acute operative loss,trauma,retroperitoneal bleed,obstretic haemorrhage like antepartum haemorrhage,post operatively-primary and secondary hemorrhage
  4. 4. Body Fluid Compartments Approximately two thirds of the body water is intracellular and the remaining one third is in the extracellular compartment which is distributed between the interstitial compartment and intravascular compartments in a 3:1 ratio
  5. 5. Compensatory mechanisms in shock 1.plasma refill 2.RAS and the hypothalamic hypophyseal adrenal system -Renin converts angiotensinogen to angiotensin1 which is metabolised in the liver to angiotensin2,a potent vasoconstrictor that stimulates aldosterone secretion,along with the pituitary release of ADH,promoting sodium and water retention.
  6. 6. Compensatory mechanisms in shock 3.Norepinephrine and epinephrine are locally and systemically released.Catecholamine mediated effects are inotropic and chronotropic resulting in increased cardiac output.They also increase the systemic vascular resistance leading to incresed diastolic pressure and therefore narrow pulse pressure. 4.Venoconstriction enhances venous return which also increases cardiac output and stroke volume.
  7. 7. Phases of shock EARLY SHOCK-The compensatory mechanisms are intact and the shock is almost eventually reversible. INTERMEDIATE SHOCK-Compicated shock associated with loss of compensatory mechanisms. LATE OR COLD SHOCK-shock is irreversible since cellular injury has occurred to the heart and brain.
  8. 8. Haemorrhagic shock Class 4Class 3Class 2Class 1 >20001500-2000750-1500<750 mlBlood loss (in ml) >4030-4015-30<15Blood volume (in%) >140>120>100<100Heart rate decreasedDecreased mean arterial pressure<60 Normal (+tilt )Normal or increased Blood pressure decreasedDecreaseDecreasedNormalPulse pressure Always delayedUsually delayedMay be delayed NormalCapillary refill Always delayedUsually delayedMildly delayednormalRespirations Essentially anuric 5-1520-30>30Urinary output (ml/hr)
  9. 9. HEMRRHAGIC SHOCK HYPOVOLEMIA LEADS TO DECREASED PRELOAD WHICH LEADS TO INCREASED SYMPATHETIC ACTIVITY AND VASOCONSTRICTION
  10. 10. Haemorrhagic shock Vasoconstriction leads to decreased mean arterial pressure and ischemia which ultimately leads to multiorgan failure-ARDS,HEPATIC FAILURE,STRESS,GI BLEEDING.RENAL FAILURE .Ischemia leads to myocardial insufficiency and severe decrease in SVR and finally death
  11. 11. Haemorrhagic shock (Early) causeSymptom or signOrgan system Decresed cerebral perfusionMental status changesCentral nervous system Adrenergic stimulation increases cardiac output and SVR.Cardiac output decreases with depressed contractility ,decreasing SVR Tachycardia,rapid thready pulse Heart(circulatory) Decreased SVR and venous return secondary to volume loss.sympathetic stimulation increases vascular tone. Normotensive or hypotensive,decreased JVD,narrow pulse pressure Systemic Decreased perfusion due t o decreased volume oliguriaRenal Sympathetic stimulation or acidosisTachypneic or normalRespiratory Vasoconstriction ,sympathetic stimulation11 Cold ,clammySkin
  12. 12. [Priorities in management:restore ORDER] O:oxygenate 6-8 litres of oxygen R:restore circulatory volume D:Drug therapy(pharmacologic support) E:evaluate response to therapy Remedy the underlying cause
  13. 13. Signs of late shock causeSign or symptom Organ system Hypoxia,worsen ing cerebral ischemia Disorientation,o -btundation CNS Irreversible ischemia,decrea sed cardiac index,decreased ejection fraction Cardiac dysfunction,tac hycardia and other arrythmias Heart RVF,extravasculDecreased JVPsystemic
  14. 14. Guidelines to manage shock >2.2L/min/m2CARDIAC INDEX Normalise A-a gradient(Pao2>30mm of Hg or SaO2>55%) PULMONARY Maintain PaO2 80-100mm of Hg,PaCo2 30- 35mmof Hg,pH>7.35 Blood gases Maintain urine output of 20-30ml/hr;normalise BU and nitrogen Renal Bilirubin<3mg/dlHepatic Restor orientationMental status
  15. 15. Evaluation of response to initial attempts at fluid resustication No response Transient response Rapid response Persistent tachycardia ,hypotensio -n ,altered mental status Transient improve- ment ,recurrence of decreased BP or increased heart rate Return to normal Vital signs
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