SHOCK

What is Shock???
Systemic state of low tissue perfusion
which is inadequate for normal cellular
respiration.
Characterized by systemic hypoperfusion
caused by reduction either in cardiac
output or in the effective circulating blood
volume.
Consequence are impaired tissue perfusion
and cellular hypoxia.
Initial cellular injury is reversible.
Become irreversible when tissue perfusion
is prolonged or severe enough that

Stages of shock
1)Non-progressive stage OR
compensated stage,
2)Progressive stage OR
decompensated stage, and
3)Irreversible stage OR
unresuscitatable shock.

1. Non-progressive stage
An initial phase during which reflex compensatory
mechanisms are activated and perfusion of vital organs is
maintained.
A variety of neurohumoral mechanisms help to maintain
cardiac output and blood pressure. These include:
baroreceptor reflexes,
catecholamine release,
activation of the renin-angiotensin axis,
ADH release, and
generalized sympathetic stimulation.
Lead to tachycardia, peripheral vasoconstriction, and renal
conservation of fluid.

2. PROGRESSIVE STAGE
Characterized by tissue hypoperfusion and onset of worsening
circulatory and metabolic imbalances.
In the setting of persistent oxygen deficit consequent to
widespread tissue hypoxia, intracellular aerobic respiration
become anaerobic glycolysis with excessive production of lactic
acid- metabolic acidosis.
Lowers the tissue pH and blunts the vasomotor response;
arterioles dilate, and blood begins to pool in the microcirculation.
Peripheral pooling worsens the cardiac output, and caused
endothelial cells were at risk for developing anoxic injury with
subsequent disseminated intravascular coagulation.
With widespread tissue hypoxia, vital organs are affected and
begin to fail.

3. Irreversible stage
Survival is not possible even if the hemodynamic defects
are corrected due to the severe cellular and tissue injuries.
Patients who are in profound shock for a prolonged period
of time become unresuscitatable.
Failure of the compensatory mechanism.
Myocardial depression and loss of responsiveness to fluid
or inotropic therapy.
Loss of the ability to maintain systemic vascular resistance
and further hypotension ensues.

Pathophysiology of shock
Cellular response to shock

 Microvascular response to shock

Tissue ischemia
Hypoxia and acidosis
Activation of complement and prime
neutrophils
Oxygen free radicals and cytokine
release
Capillary endothelial cells injury
Activation of
immune and
coagulation
system

Fluid leak out

Tissue
edema

Pathophysiology of shock
Systemic response to shock

Clinical features of shock

CARDIOGENI
C

HYPOVOLEM
IC

Classification of
shock

DISTRIBUTI
ENDOCRINE
VE
OBSTRUCTI
VE

Hypovolaemic shock
Most common.
Due to a reduced circulating volume.
Non-hemorrhagic causes:
Poor fluid intake (dehydration)
Excessive fluid loss (vomiting, diarrhea)
Urinary loss (diabetes)
Evaporation
third-spacing (bowel obstruction,
pancreatitis)

 Hemorrhagic causes:
Gastrointestinal bleeding
Trauma
AAA rupture
Ectopic pregnancy, post-partum
bleeding

Clinical signs
Agitation
Cool clammy extremities
Tachycardia
Hypotension
Narrowed pulse pressure
Weak or absent peripheral pulses
Possible decreased urine output
Decreased level of consciousness
Apparent in 25 30 % blood volume loss

Treatment to Hypovolaemic
shock
Goal: To restore the blood volume, tissue
perfusion, and oxygenation to normal as early as
possible
Replace blood volume.
Resuscitation:
Fluid therapy
Crystalloids
-Normal Saline or Ringers lactate
-Up to 2-3 times the volume lost
Colloids
-Gelofusine or 5% albumine
Blood transfusion (if >40% of blood volume is
lost OR if the patient is anaemic,Hb<8g%)

Cardiogenic shock
Occurs due to primary failure of the heart to
pump blood to the tissues, resulting in
failure to meet metabolic demands of the
cells.
Characterized by sustained hypotension
with inadequate tissue perfusion in spite of
adequate left ventricular filling pressure.
a systolic BP of <90mmHg for greater than
30 minutes
a cardiac index of <2.2L/min/m2 in the
presence of a pulmonary capillary wedge
pressure of >15mmHg.

 Causes:
AMI (most common)
Cardiac dysrhythmias
VHD
Blunt myocardial injury
Cardiomyopathy
Cardiac insufficiency

 Clinical signs:
Cool, mottled skin
Tachypnea
Hypotension
Altered mental status
Narrowed pulse pressure
Rales, murmur

Treatment to Cardiogenic
shock
Goal: Airway stability and improving myocardial pump function
Oxygen therapy: face mask/ endotracheal intubation/ ventilation
Inotropes improve cardiac muscle contractility.
Vasodilators help to dilate vessels to improve tissue perfusion.
Cardiac monitor to avoid excessive drops in blood pressure due to
use of vasodilators.
Intra-aortic balloon pump or ventricular assist devices used to
augment cardiac output.
If hypotension continues to be unresponsive,
revascularization(surgical or interventional) or valve replacement
may be considered on an emergency basis.

Obstructive shock
Reduction in preload due to mechanical
obstruction of cardiac filling.
Causes:
cardiac tamponade,
tension pneumothorax
massive pulmonary embolus or air embolus.
In each case, there is reduced filling of the
left and/or right sides of the heart leading to
reduced preload and a fall in cardiac output.

 Clinical signs:
Cyanosis
Hypotension
Experiences chest pain
Respiratory distress without
lung pathology or airway
obstuction

 Cardiac tamponade
Blood filled in pericardial sac prevents venous return to
and contraction of heart
Right ventricular compression results in a progressive
decline in right ventricular end-diastolic volume as
diastolic filling lessens, worsening cardiac output.
The central venous pressure is high, and blood pressure is
low.
Becks triad: hypotension, muffled heart sounds, raised JVP
Patient also have pulsus paradoxus where there is 10%
decrease in systolic blood pressure with inspiration.
Treatment :
Maintain preload with fluid or blood
Pericardiocentesis- aspiration of fluid from the pericardial
space that surround.

 Tension pneumothorax
Air trapped in pleural space with 1 way valve,
air/pressure builds up
Air accumulates until the intrathoracic pressure of
the affected hemi-thorax equilibrates with
atmospheric pressure, leading to complete lung
collapse or atelectasis.
Mediastinum shifted impeding venous return
Clinical features:
- Profound cyanosis, distended neck veins,
- tachypnoea, dyspnoea or respiratory arrest.
- No air entry on the side of pneumothorax, hyperresonance to percussion.
- Tachycardia, hypotension and cardiac arrest.
Treatment:

 Pulmonary embolism
Obstruction to flow through the pulmonary artery results
in increased dead space ventilation where affected lung
segments are ventilated but not perfused, observed
clinically as a substantial decrease in the end-tidal CO2
(ETCO2) that no longer reflects arterial PCO2.
V/Q mismatching is compounded by the accompanying
fall in cardiac output that results from massive PE,
leading to mixed venous desaturation.
Increased right ventricular (RV) afterload, resulting in an
increase in the RV end-diastolic volume (EDV).
The interventricular septum bows into the left ventricle
(LV) and impairs diastolic filling, resulting in decreased
LV preload and subsequently diminished cardiac output
and hypotension.
Signs: Tachypnea, tachycardia, hypoxia
Treatment : Heparin, consider thrombolytics

Endocrine shock
may present as a combination of hypovolaemic
,cardiogenic or distributive shock.

Causes of hypo- and hyperthyroidism

and adrenal insufficiency.

Hypothyroidism causes a shock state similar to that of
neurogenic shock due to disordered vascular and
cardiac responsiveness to circulating catecholamines.
Cardiac output falls due to low inotropy and
bradycardia. There may also be an associated
cardiomyopathy.

 Thyrotoxicosis may cause a high-output

cardiac failure.
Adrenal insufficiency leads to shock due to
hypovolaemia and a poor response to
circulating and exogenous catecholamines.
Adrenal insufficiency may be due to preexisting Addisons disease or be a relative
insufficiency due to a pathological disease
state, such as systemic sepsis.

Distributive shock
Can occur in the following situations:
septic shock, anaphylactic shock,
neurogenic shock
Inadequate organ perfusion vascular
dilatation
with hypotension- low systemic vascular
resistance- inadequate afterloadabnormally
high cardiac output.

Anaphylactic shock
Type I hypersensitivity
It typically causes a number of
symptoms including an itchy rash,
throat swelling, andlow blood pressure.
Common causes include insect bites
and stings, foods, and medications.
The pathophysiology include
immunologic and non- imunologic
reaction

Immunologic
immunoglobulin E(IgE) binds to theantigen(the foreign
material that provokes the allergic reaction)
Antigen-bound IgE then activatesFcRI receptors on
mast cells and basophils.
This leads to the release of inflammatory mediators such
ashistamine.
These mediators subsequently increase the contraction
of bronchialsmooth muscles, triggervasodilation,
increase the leakage of fluid from blood vessels, and
cause heart muscle depression.
Non-immunologic
Non-immunologic mechanisms involve substances that
directly cause thedegranulationof mast cells and
basophils.
These include agents such ascontrast medium,opioids,
temperature (hot or cold), and vibration. Sulfites may
cause reactions by both immunologic and non-

Neurogenic shock
Causes: spinal cord injury / anesthetic
accident /Spinal cord
failure of sympathetic outflow and
adequate vascular tone
results in vasodilation and pooling of
blood in the veins
Decrease in venous return reduces
cardiac output fainting or syncope

Treatment of Anaphylactic
Shock
Remove offending agent(allergen)
Establish an airway and return circulation(endotracheal
intubation and ventilation)

Pharmacologic support:
Epinephrine reverses peripheral vasodilation, dilates
bronchial airways, increases myocardial contractility, and
suppresses histamine/ leukotriene release

Antihistamine (chlorphenamine 10-20mg;slow IV ) stabilize

mast cells

Corticosteroids

(hydrocortisone-nt 1st choice in

emergency treatment as take several hours to block histamine
receptors) 100-300mg IV

Intravenous fluids
hypovolaemia

may also be needed to treat

Treatment of Neurogenic
Shock

Establish an airway to maintain adequate

oxygenation and ventilation
Fluid resuscitation
Inotropic support
Dobutamine
Dopamine

Atropine for severe bradycardia

High dose methylprednisolone therapy

Septic shock
Combination of distributive shock + organ
dysfunction induced by mediators of host
inflammatory response
most frequently triggered directly by G +
bacterial infections(staphylococci),
followed by G - bacteria bacilli(e.g colonic
anastomotic leak) and fungi.
Hence, an older synonym, endotoxic
shock, is no longer appropriate.

 All the hemodynamic effects of septic shock

can be produced by injection of LPS alone.
LPS + LPS binding protein CD14 receptor
activates Monocytes, Macrophages,
neutrophils produce of TNF & IL-1, induce
production of other cytokines from
endothelial cells (cytokine cascade), which
cause:
Systemic vasodilation (Hypotension),
Diminished Myocardial contractility,
Widespread endothelial injury,

3 phases
Initial extensive VASODILATION relative
hypovolaemia
2nd widespread endothelial DAMAGE
INCREASED capillary permeability + massive
fluid leakage into interstitial space --------
clinically manifest as INADEQUATE BLOOD
PRESSURE in presence of N / Increased CO

Clinical
manifestations:

Hyperthermia or hypothermia(cold sepsis)

Tachycardia
(In Septic shock the due to
Wide pulse pressure
vasodilation skin may feel warm and
Low blood pressure (SBP<90)flushed).
Mental status changes
Beware of compensated shock!---------Blood pressure may be
normal

Initial responses should include obtaining cultures of blood and

other body fluids, empiric administration of broad-spectrum
antibiotics, determination of serum lactate as a marker of
hypoperfusion, and use of intravenous fluid and vasopressor
therapy for patients with sustained hypotension.

Treatment of Septic
Shock
Removal of septic focusresection of gangrenous

bowels,closure of perforation,appendicectomy)
Earlyempiricial Antibiotics(unless u remove the
septic focus by surgical drainage of pus or
resection of gangrene,septic shock patient do not
improve)
Fluid therapy: Restoration of IV filling pressure
must be done using crystalloid(isotonic
saline/Ringers lactate) , colloids(restore IV
volume faster and remain longer in central
circulation
Vasoactive agentNEvasoconstriction and raise
in systemic VR to normal
Dopamine,dobutamine/A

Complications

Unresuscitatable shock
Multiple organ failure:
lung: ARDS
Kidney: Renal failure
Clotting: coagulopathy
Cardiac: Cardiovascular failure

 Pulm failure ARDS cerebral hypoxia

confusion and eventually COMA
Inadequate renal perfusion cause
oliguriax correctAcute tubular necrosis
and renal failure
Cerebral ischaemia cause confusion and
shock persists,reduced coronary flow and
heart failure cause death
In septic shockorgan damage is
exacerbated by intense inflammatory burst
and deterioration is inevitable unless
source of infection is eliminated.

 The acute response to sepsis is also

characterized by the release of
adrenocorticotropic hormone (ACTH),
cortisol, adrenaline, & noradrenalin,
vasopressin, glucagon, & growth
hormone.
The net result is shutdown of
noncritical systems and an overall
catabolic state.

Anti-inflammatory
factors also play an
important role in giving
rise to the compensated
anti-inflammatory
response syndrome
(CARS), in which
paralysis of the
immune system leads
to a poor outcome.

Patients with sepsis who

cycles between SIRS and
CARS are susceptible to
increased mortality.

Persons with a
heterogeneous response
are said to have a mixed