Shock

Hemorrhagic or
Hypovolemic Shock

The most common cause of shock in the surgical

or trauma patient is loss of circulating volume
from hemorrhage. Acute blood loss results in
reflexive decreased baroreceptor stimulation from
stretch receptors in the large arteries,resulting in
decreased inhibition of vasoconstrictor centers in
the brain stem, increased chemoreceptor
stimulation of vasomotor centers, and diminished
output from atrial stretch receptors. These
changes increase vasoconstriction and peripheral
arterial resistance. Hypovolemia also induces
sympathetic stimulation, leading to epinephrine
and norepinephrine release, activation of the
renin-angiotensin
cascade,
and
increased
vasopressin release. Peripheral vasoconstriction is
prominent, although lack of sympathetic effects
on cerebral and coronary vessels and local
autoregulation promote maintenance of cardiac
and CNS blood flow.

Hypovolemi Cardiogeni
a
c

Obstructive Distributive

Cardiac
output

Low

Low

Low

High

Vascular
resistance

High

High

High

Low

Venous
pressure

Low

High

High

Low

Mixed
venous
saturation

Low

Low

Low

High

Base deficit High

High

High

High

Class

Blood loss

Responce

Treatment

<15 %(0.75 l)

fast heart rate,

normal blood
pressure

Minimal

II

15-30 %(0.751.5 l)

Fast heart
rate,low blood
pressure

I.V FLUID

II

30-40 %(1.5-2
l)

Very fast HR
I.V
,low blood
fluid+packed
pressure,confu RBCS
sion

IV

>40 %(>2 l)

critical blood
pressure and
heart rate

agressive fluid
treatment

The clinical signs of shock may be evident with

an agitated patient,including cool clammy
extremities, tachycardia, weak or absent
peripheral pulses, and hypotension. Such
apparent clinical shock results from at least 25
30 percent loss of the blood volume._x0000_

Young vs old

Young healthy patients with vigorous

compensatory mechanisms may tolerate larger
volumes of blood loss while manifesting fewer
clinical signs despite the presence of significant
peripheral hypoperfusion. These patients may
maintain a near-normal blood pressure until a
precipitous cardiovascular collapse occurs.
Older adult patients may be taking medications
that either promote bleeding (e.g., warfarin or
aspirin), or mask the compensatory responses to
bleeding (e.g., blockers).
Additionally, atherosclerotic vascular disease,
diminishing cardiac compliance with age,
inability to elevate heart rate or cardiac
contractility in response to hemorrhage, and
overall decline in physiologic reserve decrease
the older adult patients ability to tolerate
hemorrhage.

Mangement

Control of ongoing hemorrhage is an essential

component of the resuscitation of the patient in
shock.

The appropriate priorities in these patients are

to

(1) secure the airway.

(2) control the source of blood loss.

(3) intravenous volume resuscitation.

Identifying the body cavity harboring active

hemorrhage will help focus operative efforts;
however, because time is of the essence, rapid
treatment is essential and diagnostic
laparotomy or thoracotomy may be indicated.
The actively bleeding patient cannot be
resuscitated until control of ongoing
hemorrhage is achieved._x0000_

Ischaemiareperfusion
syndrome

During the period of systemic hypoperfusion, cellular

and organ damage progresses due to the direct effects
of tissue hypoxia and local activation of inflammation.
Further injury occurs once normal circulation is restored
to these tissues. The acid and potassium load that has
built up can lead to direct myocardial depression,
vascular dilatation and further hypotension. The cellular
and humoral elements activated by the hypoxia
(complement, neutrophils, microvascular thrombi) are
flushed back into the circulation where they cause
further endothelial injury to organs such as the lungs
and the kidneys. This leads to acutelung injury, acute
renal injury, multiple organ failure and death.

Cardiogenic Shock
Cardiogenic shock is defined clinically as
circulatory pump failure leading to
diminished forward flow and subsequent
tissue hypoxia, in the setting of
adequate intravascular volume.
Hemodynamic criteria include
sustained hypotension (i.e., SBP <90
mmHg for at least 30 min),
reduced cardiac index(<2.2 L/min per
square meter),
and elevated pulmonary artery wedge
pressure(>15 mmHg).

Causes ofof Cardiogenic

Shock

Acute aortic insufficiency_x0000_

Acute mitral regurgitation
Left atrial myxoma
Mitral stenosis
Obstruction to left ventricular filling
Hypertrophic obstructive cardiomyopathy
Aortic stenosis
Left ventricular outflow obstruction
Septic shock with severe myocardial depression
Prolonged cardiopulmonary bypass
Severe myocardial contusion
Myocarditis
End-stage cardiomyopathy
Other causes of cardiogenic shock:_
Right ventricular infarction
Pericardial tamponade
Free-wall rupture
Ventricular septal defect
Acute mitral regurgitation from papillary muscle rupture
Mechanical complications
Pump failure

Acute myocardial infarction:_

Diagnosis

Confirmation of a cardiac source for the shock

requires electrocardiogramand urgent
echocardiography. Other useful diagnostic tests
include chest radiograph, arterial blood gases,
electrolytes, complete blood count, and cardiac
enzymes. Invasive cardiac monitoring, which is
generally not necessary, can be useful to
exclude right ventricular infarction,
hypovolemia, and possible mechanical
complications._x0000_

PHARMACOLOGICAL
SUPPORT
Inotropes: increase force of ventricular contraction,usually b-effect.

Vasopressor: constricts blood vessels, a-effect.

Vasodilator: dilates blood vessels.

Chronotrope: increased heart rate, b-effect.

Both a- and b-effects.

Inotrope, vasopressor, chronotrope.
b2-effect at low doses causes vasodilatation in
skeletal muscle, lowering SVR.
a-vasoconstrictor effect at higher doses increases
SVR and myocardial oxygen demands, with adverse
effect on cardiac output.

Adrenaline

Noradrenaline

Indicated in septic shock when hypotension due to

peripheral vasodilatation persists despite
adequatevolume replacement._x0000_

a-effect.
Vasopressor.

Dobutamine

b1 and b2.
Inotrope, vasodilator.
b1 effect increases heart rate and force ofcontraction.
Mild b2 effect causes vasodilatation.
Dobutamine and low-dose dopamine in conjunction used in
cardiogenic shock to increase BP via
increased cardiac contractility and urinary output(UO; via
increased renal perfusion).

b2 and D receptors.
Inotrope, chronotrope.
Peripheral vasodilatation, increased splanchnic blood flow and
increased renal perfusion (increased UO)._x0000_

Dopexamine
First choice inotrope in cardiogenic shock due to
leftventricular dysfunction.

Dopamine

Low dose dilates renal, cerebral, coronary and

splanchnic vessels, via D1 and D2 receptors
and b1 receptors, resulting in increased cardiac
contractility and heart rate.

High dose stimulates a-receptors, causing

vasoconstriction._x0000_

Mangement of
cardiogenic shock

Treatment of cardiac dysfunction

includes maintenance of adequate
oxygenation to ensure adequate
myocardial oxygen delivery and
judicious fluid administration to avoid
fluid overload and development of
cardiogenic pulmonary edema.
Titration of both dopamine and
dobutamine infusions may be required
in some patients.
Patients whose cardiac dysfunction is
refractory to cardiotonics may require
mechanical circulatory support with an
intraaortic balloon pump
(IABP)._x0000__x0000__x0000_

Vasodilatory Shock (Septic

Shock)
hypotension results from failure of the vascular
smooth muscle to constrict appropriately.
_x0000_In vasodilatory shock, hypotension results
from failureVasodilatory shock is characterized by
both peripheral vasodilatation with resultant
hypotension, and resistance to treatment with
vasopressors._x0000_ of the vascular smooth
muscle to constrict appropriately.
_x0000_

Other causes

Other causes of vasodilatory shock include

hypoxic lactic acidosis, carbon monoxide
poisoning, decompensated and irreversible
hemorrhagic shock, terminal cardiogenic shock,
and postcardiotomy shock._x0000_

Septic shock is a by-product of the bodys

response to invasive or severe localized
infection, typically from bacterial or fungal
pathogens._x0000_

 In

the attempt to eradicate the

pathogens, the immune and other cell
types (e.g.,endothelial cells) elaborate
soluble mediators that enhance
macrophage and neutrophil killing
effector mechanisms, increase
procoagulant activity and fibroblast
activity to localize the invaders, and
increase microvascular blood flow to
enhance delivery of killing forces to the
area of invasion. When this response is
overly exuberant or becomes systemic
rather than localized, manifestations of
sepsis may be evident.

Diagnosis
The terms sepsis, severe sepsis,
and septic shock are used to
quantify the magnitude of the
systemic inflammatory reaction.
Patients with sepsis have evidence
of an infection, and systemic signs
of inflammation(e.g., fever,
leukocytosis, and tachycardia).
Septic shock requires the presence
of the above, associated with more
significant evidence of tissue
hypoperfusion and systemic
hypotension._x0000_

Treatment

After first-line therapy of the septic patient with

antibiotics, intravenous fluids, and intubation if
necessary, vasopressors may be necessary to
treat patients with septic shock.

_x0000_patients with septic shock will develop

arterial resistance to catecholamines. Arginine
vasopressin, a potent vasoconstrictor, is often
efficacious in this setting.

Obstructive Shock
Commonly, mechanical obstruction
of venous return in trauma patients is
because of the presence of tension
pneumothorax. Cardiac tamponade
occurs when sufficient fluid has
accumulated in the pericardial sac to
obstruct blood flow to the ventricles.
The hemodynamic abnormalities in
pericardial tamponade are because
of elevation of intracardiac pressures
with limitation of ventricular filling in
diastole with resultant decrease in
cardiac output.

With either cardiac tamponade or tension

pneumothorax, reduced filling of the right side
of the heart from either increased intrapleural
pressure secondary to air accumulation (tension
pneumothorax), or increased intrapericardial
pressure precluding atrial filling secondary to
blood accumulation (cardiac tamponade) results
in decreased cardiac output associated with
increased central venous pressure.

Diagnosis and Treatment

The diagnosis of tension pneumothorax should

be made on clinical examination. The classic
findings include respiratory distress (in an
awake patient), hypotension, diminished breath
sounds over one hemithorax, hyperresonance
to percussion, jugular venous distention, and
shift of mediastinal structures to the unaffected
side with tracheal deviation.

pleural decompression is indicated rather than

delaying to wait for radiographic confirmation.
When a chest tube cannot be immediately
inserted,such as in the prehospital setting, the
pleural space can be decompressed with a large
caliber needle.

 Cardiac

tamponade results from the

accumulation of blood within the
pericardial sac, usually from penetrating
trauma or chronic medical conditions
such as heart failure or uremia. Although
precordial wounds are most likely to
injure the heart and produce tamponade,
any projectile or wounding agent that
passes in proximity to the mediastinum
can potentially produce tamponade.
Blunt cardiac rupture, a rare event in
trauma victims who survive long enough
to reach the hospital, can produce
refractory shock andtamponade in the
multiply injured patient.

 Cardiac

tamponade may also be

associated with dyspnea, orthopnea,
cough, peripheral edema, chest pain,
tachycardia, muffled heart tones,
jugular venous distention, and elevated
central venous pressure. The triad of
Beck consists of hypotension, muffled
heart tones, and neck vein distention.
Pericardiocentesis to diagnose
pericardial blood and potentially relieve
tamponade may be used. Performing
pericardiocentesis under ultrasound
guidance has made the procedure
safer and more reliable.

Thanks