1. Septic shock is caused by infection which releases cytokines that damage microcirculation and cause vasodilation and capillary leakage, leading to tissue hypoxia and multiple organ failure. Early, aggressive treatment of infection along with cardiovascular and organ system support is needed to prevent high mortality rates. 2. Hypovolaemic shock results from decreased blood volume due to blood loss, fluid loss, or fluid shifts. It progresses from mild to severe as compensation fails, leading to cellular changes, metabolic acidosis, and potentially multiple organ failure without timely fluid resuscitation and hemostasis. 3. Cardiogenic shock stems from heart failure to pump adequately due to causes like myocardial infarction, arrhythmias

1. ‫بسم‬‫هللا‬‫الرحمن‬
‫الرحيم‬

2. THE SHOCK
PROF. DR. NAWEL HUSSEIN
‫أ‬.‫د‬./‫ناول‬‫حسين‬
M.B.,B.Ch, M.S., FRCS (Ed. UK), MD
PROFESSOR OF ONCOSURGERY

3. SHOCK
 Definition: It is a state of acute circulatory
failure in which the cardiac output unable to
maintain tissue perfusion for nutrition,
oxygenation and waste disposal.
 Shock is common and the most important cause
of death among surgical patients.
 In some cases a patient may have a combination
of more than one types of shock, as in trauma
and burn, hypovolaemic and neurogenic shock
occurs at the same time.

4. SHOCK
 Types of shock:
 Neurogenic shock: this is due to peripheral
vasodilatation and peripheral pooling of the
blood.
 Hypovolaemic shock: due to decrease of blood
volume.
 Cardiogenic shock: due to failure of the heart.
 Septic shock: when infection is sever, it releases
chemical mediators which affects the
microcirculation resulting in failure of peripheral
resistance and ending in failure of the heart.
 Anaphylactic shock: due to antigen antibody
reaction that leads to failure of peripheral
resistance.

6. 1-NEUROGENIC SHOCK
 Definition:
 This is due to peripheral vasodilatation and
peripheral pooling of the blood in the skeletal
muscles and inadequate venous return, this type
is also referred to as fainting , collapse or
Vasovagal attack.
 Causes:
 Painful stimulation as catheterization or severe
trauma to the testis or to the abdomen
 Reaction to fear or fight or hearing bad news .
 Following spinal anesthesia or fracture spin
(spinal shock)
 Clinical pictures:
 Increasing pallor of the face, cold extremities.

7. 1-NEUROGENIC SHOCK
 Treatment:
 Put the patient in the shock position i.e. patient
lie flat in the bed with elevation of the lower
limbs to increase venous return and cardiac
output
 Atropine in vasovagal shock to improve
bradycardia which occurs due to increase of the
vagal tone
 Vasoconstrictors as ephedrine in spinal shock to
elevate blood pressure by increasing peripheral
resistance.
 I.V fluids if the shock persists for more than 20
minutes.

8. 2-HYPOVOLAEMIC SHOCK
 Causes:
 Blood loss: as in haemorrhage due to trauma,
operation, GIT bleeding or blood diseases.
 Plasma loss: as in burn
 Water and electrolyte loss: as in vomiting,
diarrhea high output intestinal fistula.
 Third spacing loss: the fluid is lost into the GIT
lumen and interstitial spaces as for example in
intestinal obstruction and pancreatitis.

9. 2-HYPOVOLAEMIC SHOCK
 Clinical pictures:
 Mild shock: (up to 20% blood volume loss) non
vital organs are affected as (skin, muscles and
bone)
 Pallor, cold skin
 Mild tachycardia and may postural hypotension.
 Moderate shock: (up to 40% blood volume loss)
where the kidneys, liver, intestine are also
affected, so, plus to the above manifestations,
there are:
 Tachycardia increased and hypotension.
 Oliguria or anuria (urine output of less 0.5 cc/kg/hours
indicates marked hypovolaemia.)
 Severe shock: (more than 40% blood volume loss)
brain and heart are also affected. so, plus to the

10. 2-HYPOVOLAEMIC SHOCK
 Irreversible shock:
 Progressive renal, respiratory, cardiac and CNS
decompensations.
 Acidosis: due to accumulation of acidic metabolites
 Hypothermia
 Consumption coagulopathy due to DIC
 Electrolyte disturbance as hyperkalaemia
 Multiple organ failure syndrome

11. 2-HYPOVOLAEMIC SHOCK
 Patho-physiology
 Cardiovascular and endocrine compensatory
responses:
 Aims to restores the intravascular volume, maintain
blood pressure and tissue perfusion and reduce flow to
non-vital organs to preserve flow to vital organs as
(brain, heart and kidney) by:
 stimulation of baroreceptors in carotid sinus and
aortic arch to increase heart rate and peripheral
vasoconstriction then blood pressure elevated
 Increase secretion of ADH, which leads to
vasoconstriction & oliguria, so, blood pressure
elevated
 Renal ischaemia  rennin secretion  angiotensin I
&II - vasoconstriction and aldosterone secretion
(salt & water retention)  so, blood pressure

12. EARLY COMPENSATED STAGE
(ADAPTIVE PHASE OR
NEUROENDOCRINE RESPONSE):
.1Neural reflexes:
 Stimulation of baroreceptors in wall of atria,
carotid sinus & in aortic arch → ↑ sympathetic
activity →
 Selective VC of blood vessels of skin, muscles, kidneys
& splanchnic organs → Shift of blood to heart & brain.
Vasoconstriction of veins (veins carry about 2/3 of
blood volume) will shift the blood to arterial side of
circulation.
 ↑ HR & contractility of heart.
 Stimulation of chemoreceptors in aortic arch &
carotid bodies (sensitive to minor changes in PH,
O2 tension & CO2 level) ….result in splanchnic VC
(splanchnic blood flow represents 20% of blood
volume) & coronary blood vessel dilatation.

13. 2-HYPOVOLAEMIC SHOCK
Microcirculatory changes:
 In compensated shock :
 Under the effect of catecholamines the pre-
capillary sphincters constrict  decrease of
capillary pressure  refilling from the interstitial
fluids to increase the intra vascular fluids (one
liter / hour in healthy person  increase blood
pressure.
 In de-compensated shock:
 Opening of A-V shunts leads to more capillary
ischemia and more cellular distress  release of
histamine and other chemical mediators 
contraction of post-capillary sphincter  more
slowing of the capillary flow & more ischemia.

15. 2-HYPOVOLAEMIC SHOCK
 Cellular changes:
 Hypoxia  anaerobic glycolysis  lactic acid
production (metabolic acidosis) and small amount of
energy. Body tries to correct acidosis by
hyperventilation.
 With more hypoxia  cellular functions deteriorates,
specially Na/K pump which results in increase
intracellular Na and water and increase extracellular
potassium (hyperkalaemia)

16. 2-HYPOVOLAEMIC SHOCK
 Multiple organ failure(MOF):
 MOF is defined as two or more failed organ systems
 Lung failure -- acute respiratory distress syndrome
(ARDS)
 Kidney failure  acute renal insufficiency
 Liver failure - acute liver insufficiency
 Clotting  coagulopathy
 Heart failure
 There is no specific treatment for MOF, management is
by supporting organ systems with ventilation,
cardiovascular support and dialysis until there is
recovery of organ function
 MOF currently carries a mortality rate of 60%, thus
prevention is vital by early aggressive identification
and treatment of shock.

17.  Adaptive mechanisms are very poor in
children & elderly because:
 Pediatric patients:
 Have smaller total blood volumes & therefore, they
are at risk to lose a proportionately greater
percentage of blood.
 Children < 2 years, their kidneys are immature → 
power to concentrate solute.
 Large body surface with rapid heat loss → early
hypothermia, → Coagulopathy.
 Elderly people:
 Altered physiology
 Atherosclerosis &  elastin → Poor arterial
contraction & retraction.
 Ability to respond to hypotension by tachycardia.
 Preexisting medical conditions with medications that

18. 2-HYPOVOLAEMIC SHOCK
 Measurements needed in shock:
 Urine output: urine output of less 0.5
cc/kg/hour indicates marked hypovolaemia.
 Central venous pressure (CVP):
 Normal 5-15 cm water
 Increased in: cardiogenic shock, Rt side heart failure,
fluid overload
 Decreased in hypovolaemic shock
 Swan Ganz catheter: can measure COP and
pulmonary artery wedged pressure  good
indicator of left ventricular function.
 Arterial blood gases and blood PH.
 Serum electrolytes & haematocrit value.

19. 2-HYPOVOLAEMIC SHOCK
 Treatment of hypovolaemic shock :
 Immediate resuscitation for shocked patient
is to insure a patent airway and adequate
oxygenation and ventilation, then attention
is directed to cardiovascular resuscitation.
 Fluid therapy: The mainstays of initial
treatment of shock are the infusion of fluids
 Insert two large pore cannula, blood is drawn
for typing and cross matching.
 1000-2000 ml of lactated ringer's solution
over 45 minutes. Patients can be divided into
 Responders in whom Bl.P and pulse improved
with good urine output as in only fluid loss
(intestinal obstruction) or in mild non active

20.  Transient responder  improvement then return
to previous state over 20 min, these patients
either have moderate on-going fluid losses.
 Non-responders are severely volume depleted
and are likely to have major on-going fluid losses
usually through uncontrolled haemorrhage.
 Blood: the most effective, specially with blood
loss. In patients who are actively bleeding (major
trauma, ruptured aortic aneurysm, GIT
haemorrhage) elevation of Bl.P without
controlling site of Hge., merely increase bleeding
from these sites. Thus operative Hge. control
should not be delayed and resuscitation should
be done in parallel with surgery .
 Colloid solution: in the absence of whole blood,

21. 2-HYPOVOLAEMIC SHOCK
 Pulmonary support:
 Mask oxygen for all shocked patient at high
concentration
 Evidence of respiratory failure is an indication for
endo-tracheal intubation and mechanical
ventilation.
 Position: elevation of lower limb with
maintaining the trunk in supine position
 Heating of the patient with blankets to avoid
sense of coolness.

22. 2-HYPOVOLAEMIC SHOCK
 Medications: in the form of:
 Corticosteroids: may be beneficial in these
cases.
 Sedation (morphine): relives pain& anxiety and
reduces tissue requirements for oxygen. It is
contraindicated in abdominal and head injuries
and with respiratory depression. It must be give
I.V to avoid toxicity.
 Antibiotics: third generation cephalosporines to
avoid septic complications.
 Inotropic drugs (dopamine): are used when the
condition fails to improve despite adequate
volume replacement and oxygenation. It is used
to improve myocardial contractility and increase

23. 3-SEPTIC SHOCK
 This is the most lethal shock, and considered
as one of the major killers in surgical
practice. If not well treated mortality ranged
from 25%-90%.
 Causes:
 The commonest organism is gram–ve bacteria &
its endotoxins ( part of cell wall of dead
bacteria),
 The common sources are peritonitis due to
rupture viscus, cholangitis, GIT infection &
severely infected diabetic foot.
 Predisposing factors includes, extremities of age,
DM, malignancy ,chemotherapy, corticosteroid
therapy &AIDS

24. 3-SEPTIC SHOCK
 Pathophysiology:
 Bacterial endotoxin stimulates macrophages and
Kupffer cells of the liver to release cytokines (as
: tumour necrosis factor "TNF", platelet
activation factor, prostaglandins & nitric acid) in
large amount  harmful effect on
microcirculation with capillary endothelium
damage.
 These cytokines lead to peripheral vasodilatation
and opening of A-V shunt, which lead to capillary
bypass and tissue hypoxia.
 capillary endothelium damage under the effect
of cytokines, lead to leakage of protein-rich fluid
from the circulation to the interstitial space

25. 3-SEPTIC SHOCK
 Clinical pictures:
The patient passes through two stages, the
diagnosis of the patient in the early stage
and prompt management can save the
patient.
 Hyperdynamic (warm) stage: diagnosis is
difficult and a high index of suspicion is required
to detect cases at this early stage.
 Fever (> 38oc) with warm dry skin.
 Tachycardia , hypotension & tachypnoea .
 Oliguria.
 The cardiac out-put is normal or elevated and If not
treated, patient will pass to the next stage.

26. 3-SEPTIC SHOCK
 Clinical pictures:
Hypodynamic (cold) stage:
 Sever tachycardia , hypotension & tachypnoea
 Cold clammy skin
 Restlessness and confusion
 Marked oliguria.
 Complicated by:
1. Acute erosive gastritis.
2. Systemic inflammatory response
syndrome(SIRS)
3. Adult respiratory distress syndrome (ARDS)
4. Multiple organ failure (MOF)
5. DIC and death.

27. 3-SEPTIC SHOCK
 Diagnosis: is helped by
 CBC  polymorphonuclear leucocytosis with
abundant immature forms
 High lactate level in blood
 Search for the source of infection
 Repeated blood culture at peak of fever

28. 3-SEPTIC SHOCK
 Treatment:
Treatment must be started as early as possible and
should be carried in ICU, by two arms hand by
hand, 1-control infection 2- support of body
systems with good monitoring.
1- Control of infection:
 Eradication of infection: drainage of peritonitis or
big abscess, resection of gangrenous bowel or
amputation of diabetic severely infected limb.
 Antibiotics: aggressive multiple antibiotics as
combination of (cephalosporin, garamycin and
metronidazole), till results of culture and sensitivity is
available.
 Control of predisposing conditions as DM
 Corticosteroids may have a role

29. 3-SEPTIC SHOCK
2- Support of different systems:
 The main priority is to maintain cardiovascular
system with reasonable blood pressure by:
 Fluid replacement: huge amount of ringer lactate may
be needed to replace fluid deficits till CVP reach 12-
15 mm.Hg.
 Medications (inotropes and vasopressors) if the patient
remains hypotensive despite adequate fluid
replacement as shown by CVP dopamine drip is given
to raise the blood pressure. If there is still no response
careful noradrenaline administration may be used.
 Oxygen administration is essential by mask in
mild hypoxia and by intubation and mechanical
ventilation in severe hypoxia.
 Observing urine output, and if not improved by

30. 4- CARDIOGENIC SHOCK
 Causes:
 The deficiency of tissue perfusion here is not
due to loose of blood volume but due to
failure of the heart to pump and low cardiac
output as in
1. Massive acute myocardial infarction
(commonest cause).
2. Severe arrhythmia.
3. massive pulmonary embolism
4. Cardiac tamponade.
5. myocarditis
6. High spinal anaesthesia, can cause paralysis
of the sympathetic supply of the heart.

31. 4- CARDIOGENIC SHOCK
Clinical pictures:
 Pictures of the cause
 Cold sweaty skin
 Manifestations of acute heart failure
 Dyspnea, cyanosis and pulmonary oedema.
 Congested neck veins and high CVP.
 Fall of the systolic and diastolic Blood pressure
and collapse.
 Increasing metabolic acidosis.

32. 4- CARDIOGENIC SHOCK
 Treatment:
 Oxygen should be administered
 Treatment of the cause
 Inotropic drugs as Dubotamin
 Mechanical support by intra-aortic balloon
pulsation device to elevate diastolic Bl.P, hence
better filling of the coronary arteries and
reduction of myocardial work.

33. 5- ANAPHYLACIC SHOCK
 This type of shock occurs due to Antigen
antibody reaction (allergic reaction) leads to
release of large amount of histamine which
causes capillary paralysis, dilatation and
pooling. The best example is penicillin
injection in a sensitized patient.
 Clinical pictures: Skin eruption,
bronchospasm, laryngeal oedema and
respiratory distress and collapse.
 Treatment: Immediate stop of further
injection of the causing drug , give the
patient corticosteroid injection ,adrenaline ,
antihistaminics and O2 .

34. 6- ENDOCRINAL SHOCK
 This may occur in patients with Addisons
disease or those receiving continuous
cortisone therapy if they are subjected to
any stressful situation, as infection or
surgery.
 The patient develops sever shock due to
failure of release of corticosteroids necessary
to cope with the stress from the suppressed
adrenal cortex. The result will be a state of
peripheral circulatory failure, hyponatraemia
and hyperkalaemia.
 Treatment is essentially prophylactic. Any
patient liable to this problem should receive

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