Haemorrhagic shock,

Resuscitation and Haemodynamics

Dr Lubega A
SHO Surgery
 SHOCK
DEFINITION
• A syndrome that results from inadequate perfusion of
tissues insufficient to meet the metabolic demands of those
tissues.

• Shock is a systemic state of low tissue perfusion, which is

inadequate for normal cellular respiration.

• A clinical syndrome which follows critical reduction of blood

flow within the microcirculation with inadequate tissue
perfusion and oxygen delivery to meet nutritional
requirements of cells and removal of waste products of
metabolism.
 CLASSIFICATION OF SHOCK
• Hypovolemic
Hemorrhage
Plasma volume loss

• Cardiogenic
Intrinsic
Extrinsic
• Neurogenic
• Vasogenic
Systemic inflammatory response syndrome
Infectious (septic)
Noninfectious
Anaphylactic
Hypoadrenal
Traumatic
 Hypovolemic Shock.
Causes
Hemorrhagic losses,
trauma,
gastrointestinal bleeding,
ruptured aneurysms,
fractures
 plasma volume losses

• extravascular fluid sequestration

pancreatitis,
burns, and bowel obstruction
• insensible fluid losses.
• excessive gastrointestinal, renal fluid loss
 NORMAL CIRCULATORY PHYSIOLOGY & HOMEOSTATIC
RESPONSES.
• Heart: Cardiac Output (CO) = Heart rate x Stroke
volume (depends on pre-load, contractility and
afterload).

• Blood Vessels: Arteries conduct blood; arterioles

provide resistance and control BP, veins act as
reservoir or capacitance vessels.

• Blood Volume: 5-6 L (Adult), 70 ml/kg (Child),

80ml/kg neonate
 Homeostatic Responses:

• Sympatho-adrenal :
Via baroreceptors stimulates inotropic and
chronotropic effect of cardiac contraction with selective
vasoconstriction in skin, skeletal muscles and splanchnic
circulation.

• Vasoactive Hormones:
Vasopressin constricts vascular sphincters in skin and
splanchnic organs and diverts blood to the heart and
brain. It also potentiates reabsorption of water by the
kidneys.
• Renin-Angiotensin-Aldosterone:
Results in decreased glomerular filtration and
urine output, salt and water retention and
vasoconstriction which raises blood pressure
and replenishes the vascular volume.
• Cortisol, glucagon, adrenaline:
Increase glucose concentration by several
mechanisms.
 PATHOPHYSIOLOGY OF SHOCK
•Neurohumoral responses cause increased
sympathetic activity, increased heart rate,
contractility and vasoconstriction.

•Microcirculatory changes cause fluid shift

into the vascular system.

•Depression of cell metabolism leads to

anaerobic metabolism and lactic acidosis.
 At a Cellular level
• As perfusion to the tissues is reduced, cells are
deprived of oxygen and must switch from
aerobic to anaerobic metabolism.
• When enough tissue is under perfused, the
accumulation of lactic acid in the blood
produces systemic metabolic acidosis
• As glucose within cells is exhausted, anaerobic
respiration ceases and there is failure of the
sodium/potassium pumps in the cell
membrane and intracellular organelles.
• Intracellular lysosomes release autodigestive
enzymes and cell lysis ensues.
• Intracellular contents, including potassium, are
released into the bloodstream.
• These in turn further activate the immune and
coagulation systems.
• Damaged endothelium loses its integrity and
becomes ‘leaky’. Spaces between endothelial
cells allow fluid to leak out and tissue oedema
ensues, exacerbating cellular hypoxia
• The damage to vascular endothelium with
extravasation of protein, water, sodium and
chloride results in massive oedema,
interference of microcirculatory perfusion and
cell metabolism eventually leading to multiple
organ failure(MOF) and death.
 Microvascular

• As tissue ischaemia progresses, changes in the

local milieu result in activation of the immune
and coagulation systems.
• Hypoxia and acidosis activate complement
and prime neutrophils, resulting in the
generation of oxygen free radicals and
cytokine release.
• These mechanisms lead to injury of the
capillary endothelial cells
 In haemorrhagic shock
• Haemorrhage leads to a state of hypovolemic
shock. This hypoperfused state results in
cellular anaerobic metabolism and lactic
acidosis.
• This acidosis leads to decreased function of
the coagulation proteases, resulting in
coagulopathy and further haemorrhage.

• This is exacerbated by ischaemic endothelial

cells activating anticoagulant pathways.
• Additionally, there is reduced perfusion to tissues,
and the blood supply to the gut and muscle beds
is reduced early in the compensatory process.
• Under perfused muscle is unable to generate heat
and hypothermia ensues.
• Coagulation functions poorly at low temperatures
and there is further haemorrhage, further
hypoperfusion and worsening acidosis and
hypothermia.
• These 3 factors result in a downward spiral
leading to physiological exhaustion and death
 Clinical features
• Clinically, haemorrhagic shock can be classified into the following grades:

Grade 1 15% blood volume (~750 ml) Rx Crystalloids

Mild resting tachycardia (<100), BP = Normal
Urine >30ml/h

Grade 2 15 - 30% (750=1500) Rx Crystalloids

Moderate tachycardia (>100), BP= N or low,
fall in pulse pressure, delayed capillary return, anxiety.
Urine 20-30ml/h

Grade 3 30 - 40% blood volume (1500 - 2000 ml) Rx Crystalloids

Tachycardia (>120), hypotension, poor capillary return Blood
Anxious, confused,
Urine output 5-10ml/h

Grade 4 40 - 50% blood volume (2000 -2500 ml) Rx Crystalloids

Tachycardia (>140), severe hypotension, cold, clammy skin Urgent blood
Confused, lethargic.
Anuria
• Depending on severity, symptoms and signs include
• feeling cold,
• thirsty,
• anxious,
• restless with depressed or altered mental state,
• tachypnoea,
• pallor and cyanosis,
• poor capillary refill of digits
• cold, clammy skin(warm in hyperdynamic phase)
Symptom Compensated Mild Moderate Severe

Lactic acidosis ++ ++ +++

Urine output Normal Normal Reduced Anuric

Level of Normal Mild anxiety Drowsy Comatose

consciousness

Respiratory Normal Increased Increased Laboured

rate

Pulse rate Mild Increased Increased Increased

Blood pressure Normal Normal Mild Severe

hypotension hypotension
 RESUSCITATION

• Immediate resuscitation maneuvers for

patients presenting in shock are to ensure a
patent airway and adequate oxygenation and
ventilation.
• Once ‘airway’ and ‘breathing’ are assessed
and controlled, attention is directed to
cardiovascular resuscitation
• Oxygen Delivery = (Cardiac Output) (Oxygen
Saturation) (Hb)
•  Cardiac output:
Determined by pre-load, afterload and contractility.
Administer fluids to maintain preload.
Inotropic agents: dobutamine or adrenaline.
Correct arrhythmias.

• O2 saturation: Maintain SaO2 > 90% (PaO2 = 60mm Hg)

O2- mask, nasal catheter (approx. 250-300ml/min.).
• ETT-Ventilator PEEP to decrease ventilation-perfusion
mismatch. Maintain normal pH.
•
• Hb: At > 10g/dl, early transfusion eg. 500ml PRBC
for1500 ml fluid

• Priorities: Airway- Breathing- Circulation.

•  
• Airway- Maintain a clear airway. Extend neck,
support jaw and suction.
• Administer O2 by nasal catheter or ETT
depending on severity.
• Breathing- Ensure normal breathing. Use
mechanical ventilator as indicated
 Circulation
- Stop external bleeding.
- Specific surgery to stop internal bleeding.
- Restore blood volume:

Insert large bore IV lines(14-16 gauge) or cutdown.

Crystalloids eg. 0.9% NaCl, Ringer’s lactate:
Bolus 7.5 ml/kg (0.5-2L initially in ½ - 2 hrs.).
Children: 20ml/kg as a bolus
Colloids eg. Dextran (LMWD), Hepstarch,
Haemaccel-30ml/kg
Blood to maintain Hb > 10gm/dl.
Av. 500ml PRBC for each 1500ml crystalloid.
• 3:1 rule.
• Cardiac Function: Maintain adequate blood volume to
improve CO.
(LVEDP assessed by CVP, PCWP).
Modify myocardial contractility, heart rate, rhythm.
Bradycardia: (<60/min): Atropine (0.5-1.0 mg IV).
Atrial or ventricular pacing.
Isoproterenol(1 mg in 250 ml dextrose @ 0.01-0.1
mcg/kg/min)
Adrenaline 0.1 mcg/kg/min
Life threatening: Cardioversion.
Rhythm disturbances (ECG monitor):
Treat arrhythmias with specific drugs, defibrillation
-Inotropic agents:
Dopamine(renal dose) 2-4 mcg/kg/min IVI
Dobutamine: 2.5- 10 mcg/kg/min IVI
Adrenaline: 0.1 mcg/kg/min
-Vasodilators:
eg. nitroprusside, nitroglycerine, hydrallazine.
 
 Traumatic Shock:

• Airway may be obstructed by altered consciousness,

head and face trauma, cervical injuries or foreign
bodies.
• Maintain airway by chin-lift (cervical collar for
suspected cervical injury).
• Remove secretions and protect airway from vomitus,
and blood.
• Provide airway by NTT or ETT. Use an airway.
• Alternatives include cricothyroidotomy and
tracheotomy.
• Breathing may be compromised by injury to thoracic
cage, pneumo / haemothorax or parenchymal injury.
• Stabilise chest defects, dress sucking wounds.
• Assist ventilatory effort by face mask and bag,
mechanical PPV.
• Circulation may be inadequate due to external blood
loss, fractures
• (pelvis: 1.5L, femur: 0.5-1.0L), haemothorax,
intraperitoneal or retroperitoneal bleeding.
• Prevent further external loss by direct pressure or large
dressing.
• Place patient in Trendelenburg position.
• Replace loss with crystalloids, colloids and blood
transfusions.
 Monitoring

• The minimum standard for monitoring of the

patient in shock is continuous heart rate and
oxygen saturation monitoring, frequent non-
invasive blood pressure monitoring and hourly
urine output measurements
• Monitoring for patients in shock
Minimum
■ Electrocardiogram
■ Pulse oximetry
■ Blood pressure
■ Urine output
Additional modalities

■ Central venous pressure

■ Invasive blood pressure
■ Cardiac output
■ Base deficit and serum lactate
 Damage control surgery

■ Arrest haemorrhage
■ Control sepsis
■ Protect from further injury
■ Nothing else
• Thanks for listening