Principles of Managent of

Hypovolemic Shock in a RTA

Agbarakwe Chidiebere
Table of Contents
 Introduction
 History
 Epidemiology
 Pathophysiology
 Etiology
 Clinical Features
 Management
 Causes of Death/Complications
 Conclusion
Introduction
 Shock is defined as acute circulatory failure of
sufficient magnitude to compromise tissue
perfusion
 It is the clinical manifestation of failure of

cellular function due to inadequacy tissue

perfusion & consequent cellular hypoxia
resulting from a reduction in the effective
circulating blood volume.
Introduction
 It is life threatening as cellular hypoxia and
disruption of normal metabolic function
rapidly results in irreversible organ damage
and death
 Prognosis depends on prompt & accurate

diagnosis & treatment

History of Shock
 William Brad- ford Cannon credited Hippocrates
with first use of the term ''exemia'' to describe
patients in hypovo-lemic shock

 Simeone (1964) recounts that although

circulatory failure was recognized by Ambrose
Pare in the 16th century, the first use of the
word "shock" is attributed to Le Dran in 1743
who in a monograph on gunshot wounds
implied that "choc" was a bodily re- action to
the sudden impact of a missile.
Types of Shock
 Hypovolemic shock: Collapse of Cardiac
Preload

 Cardiac Shock: Heart Pump failure

 Distributive shock: Collapse of periphery

resistance
 Septic shock
 Neurogenic shock
 Anaphylactic shock
Types of Shock
 Hypovolemic shock
 Blood loss may be internal (ruptured spleen,

ectopic pregnancy) or external, laceration

 Loss of Plasma like burns or peritonitis
 Loss of ECF: Intestinal obstruction, diarrhea,

vomiting
 Due to blood loss is Hemorrhagic

hypovolemic shock while others is Non

hemorrhagic hypovolemic shock
Types of Shock
 Cardiogenic shock: Result from failure of
cardiac ventricles to pump blood at a flow rate
sufficient to maintain body perfusion pressure.
 Distributive Shock: Due to Peripheral vessel
failure
 Include Septic shock: Bacterial toxins activate
cytokine systems & other defensive
mechanisms producing endothelial damage,
peripheral vasodilation & increased capillary
permeability
Types of Shock
 Anaphylactic shock: Type 1 hypersensitivity
reaction, antigen bind to antibody & release
histamine causes venous dilatations

 Neurogenic shock: Causes opposed vagal

tone
Pathophysiology of shock
Early Stage of Shock
 The average adult person has 4-5L" of blood (75-

80ml/kg) and 25 per cent (l,OOOml) must normally

be lost before shock appears

 Blood loss results in reduced circulating volume &

venous return and reduced Cardiac output (Starling's
Law of the Heart).

 The arterial pressure as a result is "temporarily ·

reduced, & the inhibitory afferent impulses from the
baroreceptors in the carotid sinus and aortic arch to
the vasomotor and cardioinhibitory centres are
diminished resulting in reflex stimulaion of the
adrenal-sympathetic regulators and decreased vagal
Pathophysiology of shock
 Early Stage of shock
 The increased adrenal-sympathetic activity causes:
 Increases venous constriction ,
 increasing venous return;
 increased rate of sino-atrial node,
 increased Forceful contraction of the heart and
constriction of the arterioles,
 Increased cardiac output
 while the arteriolar constriction leads to increased
peripheral resistance; raise the blood pressure to
its former value and may narrow the pulse pressure.
Pathophysiology of shock
Early Stage of Shock
 The arteriolar constriction affects splanchnic,

renal and cutaneous vessels while the

coronary and cerebral vessels dilate and
maintain adequate circulation to the heart
and brain. Adrenaline also relaxes the
bronchioles stimulate respiration
Pathophysiology of shock
Middle And Late Stages
 If the reduction in circulating blood volume

continues, decreasing the cardiac output still

further, sympathetic overactivity is maintained.
 But this mechanism by which the organism

strives to survive, may bring about its ultimate

dissolution as it further reduces tissue
perfusion, worsens the hypoxia and damages
the cells with release of inflammatory
cytokines and secondary mediators.
Pathophysiology of shock
Middle stage of shock
 Effects of vasoconstriction of the renal and splanchnic
vessels are marked. Reduced renal blood flow causes
increased production by the juxtaglomerular apparatus of
renin which activates angiotensinogen to angiotensin

 Angiotensin I is then converted to angiotensin II by ACE

released by endothelium but mainly that of the lungs.

 Angiotensin is a strong vasopressor reduces the diminished

tissue perfusion & increases release of aldosterone by the
adrenal cortex with consequent sodium retention to help
maintain ECF.
Pathophysiology of shock
Middle Stage of Shock
 Intra-renal haemodynamic shunting of blood from

the cortex to the medulla by sympathetic and

catecholamine activity increases perfusion of the
juxtamedullary long loop nephrons.

 This also increases sodium conservation. Increased

production of antidiuretic hormone following
reduction of pressure in great veins, atria, aortic
arch and carotid sinus and stimulation by the renin-
angiotensin system also increases water retention.
Pathophysiology of shock
Middle Stage of Shock
 The diminished renal blood flow results also in

diminished glomerular filtration rate and oliguria or

even anuria with consequent retention of acids and
potassium.
 Macrophages are activated to produce cytokines-

TNF,
 Interleukins which cross into the circulation &

activate the endothelial cells, tissue macrophages ,

Factor xii and complement components to produce
secondary mediators which have profound effect on
the vasculature and organs of the body.
Pathophysiology of shock
Middle Stage of Shock
 Liver hypoxia &exhaustion cause diminished synthesis of ATP
accumulation of potassium with its toxic effects on the heart, and
inability to detoxify lactate and other substances adequately.

 Excessive production of lactic acid from anaerobic glycolysis with

the carbon dioxide retention further aggravates the acidosis from
renal oliguria.

 Slowing of the circulation and leucocyte aggregation and

adherence to the vessels allow sludging of the cells in the
capillaries diminishing tissue perfusion ,acidosis,, damage of the
endothelium by TNF, released platelet factors and components of
complement predispose to microcirculatory thrombo-embolism.
Pathophysiology of shock
Late Stage of shock

 Decompensation which may take a day or more to

develop. Compensatory mechanisms break down and the
circulation fails. Markedly reduced output and rapid and
weak contraction of the heart
 Reduce the coronary perfusion with ', pooling of blood
peripherally and further reduction of venous return.

 Damaged capillary endothelium by hypoxia & increased

pressure at the venous end from heart failure , plasma
leaks through into the extravascular extracellular
compartment thereby reducing the effective circulating
still further.
Late stage of Shock
 Decreased Cerebral Blood flow
 Depressed Respiration, tissue hypoxia & lung

damage
 Further increase in the peripherally pooled

blood and decrease in the peripheral

resistance and blood pressure. Cerebral
function becomes progressively affected
resulting in confusion restlessness and finally
coma and death .
Clinical features of shock
 Class I Hemorrhage:- up to 15% volume of
blood loss.
 For otherwise healthy patients, minimal

tachycardia occurs with no changes in

respiratory rate or blood pressure internal
fluid shifts should correct the problem in
24h.
 If the patient was unstable prior to the loss,

then the patient may be symptomatic. i. V.

crystalloids should suffice.
Clinical features of shock
 Class II Hemorrhage:- 15% to 30% blood volume
loss.
 This represents about 750 to 1500ml of blood loss

in adult male. Increased sympathetic output leads to

increased heart rate and vascular tone. This leads to
tachycardia (> 100) and narrowed pulse pressure
rather than a drop in blood pressure.
 There are associated CNS changes like anxiety and

fright. Urine output remains at about 30-50ml and

hour.
 The patient may require blood transfusion after

initial crystalloid infusion.

Clinical features of shock
 Class III “Haemorrhage:- 30% - 40% blood loss.
By the time blood loss is over 2L, patients present with
the classical signs of shock. Marked tachycardia (weak,
thready pulse), tachypnoea and mental changes occur.
The systolic blood pressure falls and the patient almost
always requires transfusion.

 Class IV Hemorrhage:- More than 40% blood loss. The

patient is now nearing irreversible shock with low or
unrecordable blood pressure, barely palpable pulse and
negligible urine output. Rapid transfusion & immediate
surgical intervention to arrest haemorrhage may be life-
saving.
Features of Severe Shock

 Pulse and Blood Pressure: Increased rate of

sinoatrial node, rapid weak & thready pulse, LOW
BP.
 Cold clammy skin & Cyanosis
 Peripheral veins are collapsed
 Rapid deep respiration (air hunger)
 Confusion, restlessness, apathetic, comatose,

blurred vision
 Oliguria/ anuria
 Hypothermia
 MODS
Management
 Principles of Managing shock
 Restore tissue perfusion & oxygenation by

resuscitative measures
 Making diagnosis of etiology of shock &

administering treatment
 Continuous assessment & monitoring
Immediate Resuscitative Measures
 Oxygen therapy: Deliver 100% oxygen via face
masks or nasal prongs
 Comatose patient must be intubated and positive
pressure ventilation commenced
 Blood specimen is obtained once venous access is
got with two wide bore cannula for cross-
matching, base line haemoglobin, electrolytes,
urea, lactate, blood gases, pH and base deficit
 Intravenous infusion should be set up immediately
starting with Crystalloids at 20ml/kg or 1L in adult
fast over 30-60min (Ringers lactate)
Immediate Resuscitative Measures

 A Swan-Ganz balloon with a thermistor-

tipped pulmonary arterial catheter may be
passed with care for measuring the right
atrial and mean pulmonary arterial pressures.

 The cardiac index and mixed venous oxygen

saturation The cardiac index should be Over
4.5ml/min/m2 and the mixed venous oxygen
saturation over 70%.
Management of Hypovolemic shock
 Plasma substitute like Haemacel, Pentastarch
are preferred , they draw fluid by osmosis
from ECF to vascular compartment
 Assessment and Monitoring
 Temperature,Pulse, Blood pressure,

respiratory rate, level of consciousness are

monitored frequently
 Set up Central venous pressure line
Management of Hypovolemic Shock
 Inserting self retaining catheter for measuring
hourly urine output, 0.5-1.0ml/kg/HR in adults
and 1-2mls/kg/hr in children
 Detailed quick history to find a valuable guide
to cause of shock
 General & thorough physical examination to
search for cause of shock
 Monitor the progress of symptoms and signs
with resuscitation
 Review investigations & appropriate corrections
Drugs for Shock
Vasodilators: If after adequate fluid therapy as
shown by high C, V. P., tissue perfusion remains
inadequate-oliguria, cold skin - then vasodilator
drugs are used to improve perfusion.

(a) Dobutamine: It is inotropic and a beta

vasodilator with greater reduction in pulmonary
and systemic vascular resistance than dopamine
& better blood flow an oxygen delivery. The dose
is 2-40ug/kg/min. It is the vasodilator of first
choice.
Drugs for Shock
 Isoproterenol, a B-adrenergic drug, by causing
peripheral vasodilation, improves micro-circulation
, tissue perfusion and oxygen uptake by the cells.
It also improves the force of contraction of the
heart thereby raising the cardiac output.
Isoproterenol is also chronotropic.
It is given if the urine output remains low after
adequate replacement of the circulating blood
volume. I mg is given in 500ml of fluid
intravenously. The rate of infusion should be such
as to maintain the pulse below 120/minute
Drugs for Shock
 Dopamine, the precursor or nor-adrenaline, acts
both beta- I-and alpha-adrenergic receptors. It also
stimulates vasodilation or the renal and splanchnic
vessels and increases renal blood now, GFR , urine
Output and renal sodium excretion. It is inotropic
and increases myocardial contractility.

 At a dosage of 1-5 uglkg/min, it causes less
tachycardia and arrhythmias than isoproterenol. It is
the second drug of choice. As it has a half life - 2
min - it is given by continuous infusion, the dose
being related to the patient's response.
Drugs for Shock

 Prazosin , indoramin and chlorpromazine are

beta blockers & so cause vasodilation and
improve tissue perfusion.
Observations During Treatment
 A warm, well-perfused patient with a normal
mean arterial pressure and adequate urine
output (> 30ml/h) remains the gold standard
in monitoring. New monitoring modalities
such as stroke volume end-points,
continuous venous oxygen saturation
requiring pulmonary. artery catheter to
sample pulmonary capillary blood have not
significantly improved clinical monitoring..
 Observations During Treatment
 Frequent observation and assessment are essential.
 Clinical Signs: The patient is examined for improvement

or otherwise of tissue perfusion. As the tissue perfusion

improves:

(i) Sensorium: Consciousness is regained , anxiety and

restlessness subside, and the patient becomes calm.
(ii) Skin becomes warm and dry and the veins fill out.
(iii) The Conjunctivae and mucous membranes become
pink.
(IV) The blood in the nails fill up rapidly after finger
pressure.
Absence of these signs suggests lack of improvement.
Observations During Treatment
 Urine Output : An output of over 30ml/h
indicates adequate perfusion. In fact, the
hourly
Observations During Treatment
 Blood Pressure & Pulse are recorded every 15 minutes.
With improvement the blood pressure rises, the pulse
pressure increases and the pulse falls..
 Central Venous Pressure: The normal range of C.V .P.
 is 10-15 cm of water and fluid is given until this level is

reached.
 It must be observed that the C V.P. is a function of

several
 factors -(i) venous blood now, (ii) the tone of the main

veins,
 (iii) Distensibility and contractility of the right atrium and
 ventricle and (iv) the intrathoracic pressure.
Observations During Treatment
 Lungs and Jugular Veins: The lungs are
auscultated frequently for any evidence of
overloading. The external jugular veins are
similarly watched for raised pressure but it is
not reliable as it may be a late sign. If
overloading occurs fluids should be stopped
and diuretics given.
Observations During Treatment
 Blood paO2, pC02,HCO/anion gap, lactic acid
level,
 pH and blood sugar and pH: pO2. pC02 and

pH are estimated frequently and appropriate

measures taken. pO2 of 80mm and pC02 of
40mmHg indicate adequate oxygenation.
 The pH should be about 7.4 as acidosis is

corrected. Base deficit is a sensitive indicator

of the severity of shock and oxygen debt.
Systemic Inflammatory Response
Syndrome(SIRS)
It is a term introduced at a consensus meeting of the
American College of Chest Physicians and Critical Care
Medicine in 1991 on sepsis

It is a syndrome characterized by two or more of the

following clinical criteria:
1. Temperature >38°Cor <36°qrectal)
2. Heart rate >90 beats per min.
3. Respiratory rate> 20breaths/min. or PaCO2 < 32mmHg
4 WBC > 12.000mm3 or <4,OOOmm3 or > 10% immature
Band forms.
Systemic Inflammatory Response
Syndrome(SIRS)

Causes include infections ( bacteria, viruses, fungi.

protozoa) and non-infectious conditions (acute
pancreatitis.
burns, trauma, hypovolaemic shock. autoimmune
disease, drug fever), Gram-negative bacteria account
for 50-60% and Gram positives or35-40%.

Following tissue injury by microbial, mechanical,

chemical.
or thermal stimuli, there is a local inflammatory reaction
during which humoral and cellular responses are
activated to localize the infection/tissue damage
Systemic Inflammatory Response
Syndrome(SIRS)

Later the cells produce and release anti-inflammatory cytokines

such
as IL-4 and lL-1O to inhibit the activity of the
pro-inflammatory cytokines and so Iimit their possible harmful
effects..

These cytokines act in paracrine and autocrine fashion stimulate

Secondary mediators from arachidonic acid metabolites e.g.
prostagandins. PAF. thromboxane A2 etc. This may lead to
SIRS. Progression of the process leads to the septic shock which
May result in the dysfunction of several organs -Multiple Organ
Dysfunction Syndrome -
Causes of death in shock

1 Pulmonary insufficiency
2. Cardiac failure/arrest
3. Cerebral failure
4. Pre-renal failure/ATN
5. Metabolic acidosis
6. Sepsis/SIRS
7. Liver failure
8. Failure of coagulation and immune systems.
9. Multiple Organ Dysfunction Syndrome
Conclusion
Hypovolemic Shock is a surgical emergency
that should be handled with urgency &
precision to prevent mortality & morbidity.