SHOCK AN OVERVIEW

Definition a multifaceted syndrome

leading to systemic & localized tissue
hypoperfusion, resulting in cellular
hypoxia & multiple organ dysfunction

DESCRIPTION

1. Perfusion may be decreased with obvious

signs such as hypotension
2. Perfusion may be decreased due to
maldistribution as in septic shock where
systemic perfusion may appear elevated
3. Signs of malperfusion may be subtle & lead to
significant organ damage
4. Prognosis determined by degree of shock,
duration, No of organs affected, previous
organ dysfunction & ? Genetic predisposition

ETIOLOGICAL CLASSIFICATION
Hypovolemic
Loss of circ intravascular vol & decrease in cardiac
preload
May be hge- trauma, GI bleed, nontraumatic internal
bleed (aneurysm, ectopic rupture) or bleeding PV
Nonhgeic fluid loss from GI tract ( vomiting,diarrhea,
fistula), urinary losses (DM), evaporative (fever,
hyperthermia) & internal fluid shifts(3rd space loss as
in intestinal obstruction)
Clinical signs depend on volume lost & rapidity of loss
Most common form
All forms have a component of decreased preload

Contd

Obstructive
Mechanical obstruction to normal cardiac
output causing decrease in systemic
perfusion
Cardiac tamponade, tension pneumothorax.
Clinical signs raised JVP, muffled heart
sounds & decreased breath sounds
massive pulmonary embolism & air embolism

contd

Cardiogenic
Caused by myocardial (pump) failure
Extensive myocardial infarction most common
cause
Reduced contractility (cardiomyopathy, sepsis
induced), AS, MS, atrial myxoma,
dysrhythmias

contd

Distributive
Caused by systemic vasodilatation (infection,
anaphylaxis) resulting in systemic hypotension &
inc / dec CO
SIRS most common cause of distributive shock
Most common cause of SIRS is epsis
Despite the high CO there is cellular hypoxia
due to disruption of mitochondrial function
Anaphylaxis, severe liver dysfunction, neurgenic
shock (spinal trauma) also cause distributive
shock

contd

Endocrine shock
Hypothyroidism, hyperthyroidism with cardiac
collapse, adrenal insufficiency
Adrenal insufficiency may be a contributor to
shock in critically ill patients. Case
unresponsive to treatment should be tested
for adrenal insufficiency.

PATHOPHYSIOLOGY
Result of shock decreased tissue perfusion &
cellular hypoxia
Cell hypoxia-cellular ischemia, alteration in Ca,
cAMP & formation of OFR
Hypoxia enhanced vasc permiability & dec
control on memb tpt fns
Reperfusion release of OFR cell
damage
Neutrophil activation & release of
proinflammatory cytokines

contd

Further cell damage, third spacing,

activation of coag, microcirc thrombosis,
collapse & further ischemia
In sepsis & SIRS initial event is
inflammatory response
Microcirculatory collapse leads to MOF

DIAGNOSIS
Vital signs- HR, BP, temp, urine output,
SpO2 traditional measures
50-85% of patients with normal or near
normal values are still in shock
Hypotension & narrow pulse pr sign of
severe vol loss
MAP better guide to therapy
Hypothermia indication of severe hypovol &
septic shock

contd

Urine output end organ response to shock,

1-2 hrs needed to measure
SpO2 early indicator of hypoxia, may be
invalid in hypothermic pt
Invasive hemodynamic monitoring better
ABP, CVP, PAC,SvO2, Oesophageal
doppler, Flowtrac, lidco, picco

RESUSCITATION END POINTS

Lactic acid production
Cells with inadequate O2 will switch to
anaerobic metabolism
lactic acid byproduct of anaerobic met
elevation of lactate is measure of severity of
shock. Lactate also elevated in liver & kidney
failure, ARDS
Rate of clearance of lactate a better marker
for adequate resuscitation

contd

Base deficit
Base deficit is amt of base required to titrate
whole blood to a normal pH
Elevated base deficit correlates with severity
of shock
correction of BE is a guide to further mgnt

Intra mucosal pH monitoring

Mesentric hypodynamic response to shock
Gastric tonometry measures intramucosal pH
& is an early indicator of gut hypoperfusion,
correlates with mortality
Technically difficult less used

TREATMENT
Rapid recognition & restoration of perfusion
is key to preventing multi organ failure &
death. In all forms of shock rapid
restoration of preload with fluids is the 1 st
treatment
Treat shock while identifying its cause
Further treatment depends on etiology

contd

Hypovol shock
Rapid infusion of large vol of fluids thru large
bore IV cannulae, central access may be
needed ( incl PAC)
If cause be, then after initial 2-3 ltrs of fluids,
blood is transfused
Recent data supports use of packed cells :
FFP : platelets in a 1;1;1 ratio
Factor VIIa may also be useful
Resuscitation complete only when base excess
& lactate corrected to acceptable levels
Vasoconstrictors rarely needed

contd

Obstructive shock
Identify cause & relieve early
Pericardiocentesis, pericardiectomy for
tamponade
Needle decompression , tube thoracostomy
for tension pneumothorax
Ventilatory, cardiac support, thrombolytics &
heparin for PE

contd

Cardiogenic shock
Optimise preload with infusion of fluids
Optimize contractility with inotropes, balancing
cardiac O2 demand
Adjust afterload to maximise CO. pts may
need vasodilation to decrease SVR
Diuresis may be indicated
Underlying cardiac cause needs treatment
PAC is recommended to guide therapy

contd

Distributive shock
In SIRS & sepsis , shock due to toxins/mediator
induced vasodilatation
Aggressive fluid resuscitation
Pressors after infusion of volume
Dobutamine, nor-adr, vasopressin
Low dose steroids if evidence of adrenal
insufficiency
Treat underlying cause of SIRS