Dr.

Marinna Scarlett
Department: Surgery, Radiology,
Anaesthesia & Intensive Care

Year 2 MBBS Students October 2012


A state of generalized inadequate tissue
perfusion due to cardiac or non-cardiac
pathology

It is a state in which there is severe
circulatory impairment and/or organ
dysfunction such that the metabolic needs
of the tissues and organs are not met.







These metabolic needs include delivery of
substrate e.g. 0
2
and nutrient and removal
of metabolic wastes (CO
2
, urea etc.).

If these needs are not met, organ
dysfunction and death will occur.

Shock is usually accompanied by
hypotension but hypotension can exist
without shock.
Hypovolaemic
Septic
Cardiogenic
Anaphyllactic/Anaphyllactoid
Spinal
TYPES OF SHOCKS:
Hypovolaemic Shock
Commonest type
Due to intra-vascular depletion 2
0
to
- haemorrhage (as in trauma or
surgery)

- other fluid loss e.g. vomiting,
diarrhoea, burns, excessive UO
(Diabetus Mellitus & Insipidus)

Hypovolaemic Shock
Losses within the body due to various
diseases e.g.
- intestinal obstruction
- pleural effusion
- ascites
- internal hemorrhage (e.g. ruptured
ectopic pregnancy, liver, spleen latter
two due to trauma
Clinical manifestations:
Pallor ( especially in cases of blood loss)
Cyanosis
Sweating
Tachycardia
Hypotension
Tachypnea
Oliguria

CV Collapse with cold clammy skin, cardiac
dysrhythmias or arrest and impaired consciousness
confused/obtunded/unresponsive
physiologic responses
The bodys normal homeostatic reflexes are
geared to:-

maintaining and restoring the intra-vascular
volume, blood pressure and vital organs
perfusion.

Increase SNS activity causes the release of
catecholamines (adrenaline, NA and
Dopamine)

physiologic responses

Decrease renal blood flow causes increase
renin and Anti-Diuretic hormone (ADH)
release increase water absorption by the
collecting ducts.

Renin-Angiotensin system is activated
increase sodium and water absorption from renal
tubules cause increase intravascular volume
If loss is not continuous

physiologic responses:
Catecholamines causes:-

in HR and BP normal or subnormal

If subnormal decrease blood flow to kidneys,
intestine and musculoskeletal organs

BF to kidneys oliguria or anuria renal
impairment

BF flow to the intestine & skin can lead to
ischemia if prolonged.
Clinical manifestation:

Blood flow to the vital organs:-

brain
heart
lungs
liver

will be maintained until blood loss is >20%
of the blood volume



>40% intra-vascular loss is associated with
cardio-vascular collapse/shock
Person/patient is now moribund
Parameters to monitor
to assess severity:
blood loss measure if can
Vital signs/parameters PR, BP, UO,
CVP, conscious level.

Importance of resuscitation (fluid and/or
cardiac and pulmonary) ASAP
& before anaesthesia and surgery.

Parameters to monitor
to assess severity:
Importance of resuscitation (volume and/or
cardiac and pulmonary) ASAP
& before anaesthesia and surgery.

Anaesthesia will result in loss of sympathetic
reflexes and tone dramatic CV collapse
cardiac arrest
The key to therapy:
Restore intra-vascular volume and hence
blood flow to all organs system.

This requires:
Aggressive fluid therapy crystalloid,
colloid and blood for replacement of
deficit and continued loss
via at least 2 large bore IV cannula.
The key to therapy contd:
Control of blood loss if possible compression
dressing, suturing of wound/s, long bone
stabilization, emergency surgical intervention
(e.g. laparotomy) etc.

Trendelenburg position (head down)
+/- elevation of feet.

External cardiac massage and ventilation
(CPR) may be necessary.
Septic shock:
Cause Gram-negative bacteria or
endotoxin released. May also be triggered
by GP bacteria.

{Endotoxin is a part of the outer
membrane of GNB. It is a heat stable
lipopolysaccharide}
{Exotoxin is a high molecular weight, heat
labile antigenic protein}.

Septic shock:
The relationship between delivery and
uptake is disturbed, with delivery being
increased (in the early stage), but uptake
decreased.

There is defect in O2 uptake and excretion
of metabolic waste

Septic shock- Sources of
Infection:
CNS:-
meningitis
cerebral/cerebellar abscess
infected spinal cord haematoma

Facio-maxillary/ENT:-
infected sinusitis
severe gingivitis

Respiratory system:- Pneumonia
Septic shock- Sources of
Infection:-
:
GIT
perforated viscous/organ diseased or
trauma stabbing, gun shot,
laparoscopy or laparotomy

biliary system disease (gall stones or
infection) with subsequent perforation

translocation of bacteria from the GIT in
patients who are NPO for prolong period

Septic shock- Sources of
Infection:
Urogenital system:-
instrumentations perforation during
cytosocpy

UTI - may be a late complication of
trauma , instrumentation or diseases
process (hypertrophied prostate, urethral
stricture).

Muscular-skeletal:- infection e.g. septic
arthritis, infection of muscle, bone/s or skin




Clinical features:
Ill-looking, febrile, tachycardia
(increase in pulse volume in the early stage)

Normal or decrease BP
flushed face due to vasodilatation
warm dry peripheries due to decrease in SVR
increase in CO
Temperature >38 or <36
0
C.
Clinical features:

There is usually an obvious clinical site of infection
LTRI
large bowel
biliary
genito-urinary system
Long bone/joint infection

leucocytosis (esp. neutrophilia) or leucopaenia
Full septic screen - Cultures (esp. blood, urine,
sputum, infected wound, spinal fluid etc.) *
SIRS contd

Elevated WBC does not distinguish between
infected and non infected state.


C-reactive protein (CRP) is a better indicator
of the presence of infection in trauma patient

Suggest infection esp. if it remains elevated after
day 4 post injury.
Clinical features:

SS occurs because the bacterial and/or products
trigger a complex network of cytokines released
by macrophages, neutrophil, endothelial and
other inflammatory cells within the body.

Causes fueling of the systemic
inflammatory response syndrome (SIRS).

Pathophysiology of sirs
The central mechanism in initiating SIRS is the
abnormal secretions of Inflammatory mediators
cytokines (C ), triggered by bacterial products,
shock, severe burns and trauma.

Cytokines are peptides and glycoproteins which
function as intra-cellular mediators and normally
regulate many biologic processes, including local
And systemic immune responses, inflammation,
Wound healing and haematopoiesis.
Important mediators in severe
sepsis:
Cytokines
Complement System (CS)
Contact system and extrinsic pathways of coagulation
Fibrinolytic System
Cell (e.g. mononuclears, macrophages, microphages
(predominantly neutrophils), endothelial cells and
platelets
Prostaglandins (PG)
Leukotrienes (LT) & Interferon (IF)
Oxygen free radicals proteases
Nitric Oxide (NO)
Clinical features:
Advanced disease state:-

mal-distribution of blood flow to tissues

Myocardial depression may occur
(direct/indirect effect of endotoxins).

The greatest threat in the late stage is the
refractory hypotension that may occur.

Clinical features:
Advanced disease state:-

Hepatic
Cerebral
Renal failure will occur

if the disease is not halted

(Multi-organ failure - MOF).
1
0
goal of Treatment:
Restore normal blood & O
2
supply to tissues.

Intra-vascular volume must be restored
Adequate oxygenation of the blood and delivery
of O
2
to tissues
Abate the SIRS.

Fluid, O
2
therapy, Rx. infection aggressively
appropriate antibiotics * +/- surgical intervention
1
0
goal of rx:
To restore normal blood & O
2
supply to tissues.

Cardiac support +/- inotropic agents esp.
vaso- constrictor agents (Noradrenaline).

ventilatory support may be necessary

Decrease O
2
demand by abating/treating:-
Fever
Severe tachycardia
Dysrhythmias

Monitor
CVS
ABGs, pH, serum lactate, urea, electrolytes (as
well as the clinical parameters)

Improvement in these is a sign of improvement of
O
2
supply-demand balance.

Gastric intra-mucosal pH is advocated by some
clinicians.
TREATMENT

Steroids and activated protein C (Xigris)- To
decrease inflammation

Steroids: Hydrocortisone & Fludrocortisone

IL inhibitors have also been tried but with
limited success.

Vasopressors- dopamine, NE, pitressin

Cardiogenic shock
Heart pump failure
Refractory IHD
MI, CCF, Valve Failure

Cardiac tamponade, cardiomyopathy,
Hypertension HTN induced LVF, AIDS


Clinical features:
BP
PR
JVP
CVP
Peripheral edema may progress to
anasarca
Enlarged liver
UO

management:
Rx
Preload Rest, Diuretic, fluid
restriction.

Contractility Inotropic agent/s,
coronary vessel dilators.

After-load Anti hypertensive agents,
vasodilators.
Ventricular assist device
Anaphylactic/
anaphylactoid shock
Former Previous exposure to antigen & is
IgE mediated

Latter No previous exposure to antigen & is
non- IgE mediated.
Clinical features:
Skin Rash, wheals, erythema, urticaria.

CVS Sudden hypotension & tachycardia

RS Bronchospasm, laryngospasm.
Management
Stop the infusion of the suspected agent

Call for help

Maintain airway institute BLS

Administer 100% O
2

Ensure adequate breathing

Patient may need to be intubated

Management contd.
Adrenaline 1 ml of 1:10,000 (0.1mg/ml)

Repeat as necessary

Support CVS fluid & ECM.


These are the 1
0
Rx.

Management contd.

2
0
Rx includes:-

Anti-histamine H1 + H2,

Hydrocortisone,

Salbutamol or other bronchodilators.

Cardiovascular support as needed
Spinal shock
Seen with high SC injury (C3-6) and
results from mechanical disruption of
sympathetic NS outflow.

This results in marked vasodilation
there is loss of ability to
vsoconstriction.
Clinical features:
Patient feels:
warm and *dry to touch,
slow pulse* despite being relatively
hypotensive.

They are functionally hypovolaemic since the
intra vascular capacity is now greater than the
IV volume volume : capacity mismatch.

management:
Cardiovascular & respiratory support &
protect against hypothermia

fluid therapy (elevation of legs)

atropine, (ephedrine) to counteract
bradycardia

inotropic vasoconstrictor agent (e.g.
noradrenaline, phenylephrine, metaraminol)

.
SPINAL INJURY
NB. Spinal injuries will affect breathing, if
injury is high C3-C4.

Innervation of the diaphragm is disrupted. These
will need tracheal intubation and mechanical
ventilation.

Spinal cord oedema will take 6/52 3/12 to
resolve. Spinal cord disruption leads to
permanent paralysis +/- permanent dependency
on a ventilator.
SPINAL INJURY

Rx for spinal injury methylprednisolone
30mg/kg stat then 5.4mg/kg/hr x 24-48 hrs.

There must be a high index of suspicion.
Assumed SCI until proven otherwise, esp. in
acceleration de-acceleration injuries (e.g.
falls from height, MVA/RTA).

SPINAL INJURY

Spinal stabilization

Philadelphia cervical collar
Manual-in-line stabilization
Care with movt. and intubation
log rolled - keeping head and neck stable and
moving head, neck and trunk as one unit












The UHWI
Pathophysiology of sirs
The central mechanism in initiating SIRS appears to
be the abnormal secretions of Inflammatory mediators
cytokines (C ), triggered by bacterial products,
shock, severe burns and trauma.

Cytokines are peptides and glycoproteins which
function as intra-cellular mediators and normally
regulate many biologic processes, including local and
systemic immune responses, inflammation, wound
healing and haematopoiesis.
Pathophysiology of sirs
The most important C are TNF (esp. TNF and
interleukin-1 (IL-1). Others include IL-6, 8 and
interferon.

Specific receptors have been discovered
for these C, as well as specific binding protein for
endotoxin these are anchored protein for attaching
endotoxin to the specific receptor. Macrophages etc.
synthesize and release TNF following exposure
to triggering substances.
SIRS
SIRS is the inflammatory state (the bodys
response) seen with various forms of clinical insults
(severe infection sepsis, haemorrhagic shock,
severe trauma and burns).

Severe infection is the commonest cause.

Features:- elevated temperature and WBC.

The hallmark is a hyperdynamic physiologic state.
TREATMENT Goal
CVP 8-12 mmHg
PCV > 30%
Sv02 > 70%

IABP
May be useful in cardiogenic shock esp. if ass.
with MI.

CAP = ADP LVEDP
CAR
ADP = Ao. Diastolic Pressure
CAR = Coronary Artery Resistance