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Type

Hypovolemic
- less baroreceptor
stimulation from stretch
receptors = less inhibition of
vasoconstriction
- increased chemoreceptor
stimulation of vasomotor
centers
CAUSES:
Increase VC & peripheral
arterial resistance
increase SY stimulation
( NE, E, ADH, RAAS)
*No SY effects on cerebral
& coronary vessels

Causes
- intravascular volume depletion
(haemorrhage)
- extravascular sequestration of
plasma volume (ascites, peritonitis)
- GI, GU, sensible losses (intestinal
obstruction, heat)

Manifestations
Hypoperfusion
- low blood volume
- low cardiac output
- increased peripheral
vasoconstriction (compensatory
increase in cardiovascular
adrenergic discharge)

Diagnosis
1.
2.

* flow to skin is sacrificed first then


kidneys & viscera, then heart & brain

Manifestations expected with 2530% blood loss:


- cool clammy extremities
- tachycardia (110-120bpm)
- weak or absent peripheral
pulses
- hypotension
- oliguria???
30% loss:
Mild tachycardia
Tachypnea
Anxiety
40% loss:
Requires immediate
operative intervention

Serum lactate & base


deficit
Tissue hypoperfusion
O2 debt
Severity of hemorrhagic
shock
ABG: measure tissue
acidosis

*moderately severe & severe


shock = easy to recognize, early
or mild hypovolemic shock = signs
of adrenergic discharge to skin are
subtle and difficult to detect
- monitor urine output + serial
hematocrits + postural changes in
BP

Sites that cause extravascular


blood volume loss ->
hypotension:
External
Intrathoracic
Intraabdominal
Retroperitoneal
Long bone fractures
In nontrauma px: GI tract
Pleural cavity: can hold 2-3 L
of blood
Intraperitioneal hemorrhage:
most common source of blood
loss inducing shock (dx:
through ultrasound &
diagnostic peritoneal lavage)

Treatment
Priority:
Secure airway
- lower head w/ support of jaw +
administration of supplemental oxygen
- for those with airway obstruction:
trachea should be intubated, mechanical
ventilation initiated
Control source of blood loss
IV volume resuscitation
- cannot be done until hemorrhage is
controlled
- initial resuscitation: administer
nonsugar, nonprotein crystalloid solution
w/ electrolyte composition approximating
that of plasma or hypertonic saline
Aims it to keep sys BP at
90mmHg
- if hemorrhage is severe, use blood
products (fresh frozen plasma)
**if patient is unresponsive to initial
resuscitation, there is still ongoing active
hemorrhage.
**minimize heat loss & maintain
normothermia
Hypothermia is associated with
acidosis, hypotension, coagulopathy

Type

Traumatic
May be due to:
- soft tissue injury
- long bone fractures
- burns
Hypoperfusion is
MAGNIFIED by
proinflammatory activation!

Causes
- due to external and internal
volume losses (loss of blood from
wound externally and loss of blood
into damaged tissues)
- worsened due to plasma
extravasation into tissues and
organs distal from injured areas
(due to a generalized systemic
intravascular inflammatory
response)

Ex. Small volume hemorrhage +


soft tissue injury or any
combination of hypovolemic,
neurogenic, cardiogenic,
obstructive shock = precipitates
proinflammatory activation

Manifestations

Diagnosis

Treatment
Treatment plan:
Prompt control of hemorrhage
Adequate volume resus. To correct
O2 debt
Debridement of nonviable tissue
Stabilization of bony injuries
Appropriate treatment of soft tissue
injuries

Others:
Administration of a balanced salt
solution (several liters)
If BP does not respond promptly:
Vasoconstrictors
To restore venous tone
Vasoconstriction of systemic
arterioles = increased BP
*body temp must be monitored &
excessive heat loss prevented

Type

Septic/ Vasodilatory
-

Final common pathway


for profound &
prolonged shock
Development of a
hypermetabolic state

Causes
- dysfunction of the endothelium &
vasculature secondary to
circulating inflammatory mediators
and cells
- as a response to prolonged and
severe hypoperfusion (failure of
vascular smooth muscle to
constrict appropriately)
Causes:
- systemic response to infection
(by product of the bodys response
to disruption of host-microbe
equilibrium resulting in
invasive/severe localized infection)
- hypoxic lactic acidosis
- CO poisoning
- decompensated, irreversible
hemorrhagic shock
- terminal cardiogenic shock
- non-infectious systemic
inflammation
- pancreatitis
- burns
- anaphylaxis
- acute adrenal insufficiency

Manifestations
Manifestations:
Peripheral VD + resultant
hypotension + resistance to
treatment with vasopressors
Enhanced CO
Fever (due to
hypermetabolic state)
Leucocytosis
Hyperglycemia
Tachycardia

Diagnosis
Sepsis: infection +
inflammation
Severe sepsis: hypoperfusion
+ signs of organ dysfunction
Septic shock: above +
systemic hypotension

1.
2.
3.

4.
VD in septic shock due to:
Upregulation of the inducible
isoform of NOS in vessel
wall = increased amounts of
NO for sustained periods of
time
Renders vasculature resitant
to vasoconstrictors
Signs of hypoperfusion:
Confusion, malaise, oliguria,
hypotension

5.

Treatment
Assessment of adequacy of
airway and ventilation
Fluid resuscitation + restoration
of circulatory volume w/
balanced salt solutions
Use catecholamines =
vasopressors
o Patients with SS are
resistant to catecholamines
-> use Arg vasopressin
Manage hyperglycemia
(intensive insulin therapy)
Corticosteroids
o Improved MAP in response
to NE
o Patients with SS are
believed to have adrenal
insufficiencies

Type

Cardiogenic
-

Circulatory pump
failure = diminished
forward flow + tissue
hypoxia

Causes
Most common cause: acute,
extensive MI
Vicious cycle:
Myocardial ischemia -> myocardial
dysfunction -> more myocardial
ischemia
Ex. LV damage = low SV
Low CO/contractility with an
adequate intravascular volume will
lead to underperfused vascular
beds + reflexive SY discharge
(increase in HR, Fc, O2
consumption)

Manifestations
Manifestations:
Sustained hypotension
(<90mmHg for at least
30mins)
Elevated pulmonary artery
wedge pressure
Cool & mottled skin
Tachycardia
Diminished pulses

Diagnosis
Present with clinical
findings associated with
discharge of the
adrenergic nervous
system and release of
angiotensin and
vasopressin
If caused by R vent
dysfunction:
o Neck veins are
distended
If caused by L vent
dysfunction:
o Px has rales +
3rd heart sound
or ventricular
gallop rhythm
(usually heard at
the end of
diastolic vent
filling)
If dysfunction is
chronic/severe, px may
present with the ff:
enlarged heart, distended
neck veins, etc

1.
2.
3.

Treatment
Airway and ventilation
Support of circulation
Treatment of cardiac dysfunction
o Maintenance of adequate
oxygenation = ensure
myocardial O2 delivery
o Judicious fluid
administration = avoid fluid
overload & cardiogenic
pulmonary edema
o Treat dysrhythmias &
cardiac block
o Inotropic support
(more on p.106)

Type

Obstructive

Causes
Mechanical obstruction of
venous return
o Due to tension
pneumothorax
o Cardiac tamponade:
sufficient fluid has
accumulated in
pericardial sac to
obstruct blood flow to
ventricles
IVC obstruction
o DVT
o Neoplasma
Increased intrathoracic
pressure

Manifestations
Hemodynamic abnormalities:
Due to increased
intracardiac pressures,
ventricular filling is limited =
low CO
Determinants of degree of
hypotension:
1. Increased intrapleural
pressure due to air
accumulation (TP)
2. Increased
intrapericardial pressure
due to blood
accumulation (CT)
= low CO = increased central
venous pressure

Diagnosis
Tension pneumothorax:
Respiratory distress
Hypotension
Diminished breath
sounds
Hyperresonance
Jugular venous distention
(may be absent in
hypovolemic px)
Shift of mediastinal
structures to unaffected
side with tracheal
deviation (usually late
finding)
Cardiac tamponade:
Dyspnea
Orthopnea
Cough
Peripheral edema
Chest pain
Tachycardia
Muffled heart tones
JV distention
Becks triad for CT:
hypotension, muffled heart
tones, neck vein distension

Treatment

Type

Neurogenic
-

Diminished tissue
perfusion as a result of
loss of vasomotor tone
to peripheral arterial
beds
o Increased
vascular
capacitance
o Low venous
return
o Low cardiac
output

Causes
Spinal cord trauma
Spinal cord neoplasm
Spinal/epidural anesthesia

Manifestations
Manifestations:
Bradycardia (because there
is no SY discharge)
o SY activity/input is
disrupted = prevents
reflex tachycardia that
occurs with
hypovolemia
Hypotension
Cardiac dysrhythmias
Low CO
Low PVR
Warm extremities (loss of
peripheral VC)
Motor and sensory deficits

Diagnosis
-

Treatment
Restoration of intravascular volume
alone
Administration of vasoconstrictors
(as long as hypovolemia is excluded
as cause of hypotension)
o If patient is unresponsive,
give dopamine.