SHOCK

ROLANDO E. CABATU, M.D.

UST Department of Surgery

 Definition of terms
Types of Shock
Diagnosis
Signs/symptoms

Prevention
Management
Complications
Endpoint of Resuscitation

DEFINITION
a failure to meet the
metabolic demands of cells
and tissues and the
consequences that ensue.
inadequate tissue perfusion
inadequate removal of cellular
waste products

RECOGNITION
Blood pressure
pulse rate
Pallor

Temperature
Mentation
Urine output
Central Venous Pressure / PCWP

A. Cardiogenic shock due to

extrinsic causes
B. Cardiogenic shock due to
intrinsic causes
C. Hypovolemic shock
secondary to blood loss
D. Hypovolemic shock
secondary to third space
losses
E. Hypovolemic shock
secondary to insensible
losses
F. Septic shock
G. Neurogenic shock

1. A 19-year-old man presents to

the emergency department by
ambulance with a stab wound
adjacent to the left nipple
region. His blood pressure is
50/30 mm Hg and he is
unresponsive.

A. Cardiogenic shock due to

extrinsic causes
B. Cardiogenic shock due to
intrinsic causes
C. Hypovolemic shock
secondary to blood loss
D. Hypovolemic shock
secondary to third space
losses
E. Hypovolemic shock
secondary to insensible
losses
F. Septic shock
G. Neurogenic shock

2. A 23-year-old medical student

suddenly becomes faint and
dizzy while observing a right
inguinal hernia repair in the
operating room. The student
collapses and during evaluation
is noted to have a blood
pressure of 85/50 mm Hg.

A. Cardiogenic shock due to

extrinsic causes
B. Cardiogenic shock due to
intrinsic causes
C. Hypovolemic shock
secondary to blood loss
D. Hypovolemic shock
secondary to third space
losses
E. Hypovolemic shock
secondary to insensible
losses
F. Septic shock
G. Neurogenic shock

3. A 42-year-old, obese woman

presents with a 23 day history of
persistent nausea and vomiting. Her
blood pressure is 80/50 mm Hg with
a heart rate of 140 beats/min. She is
noted to have an unreducible
umbilical hernia on examination.
Abdominal radiograph reveals a
high-grade small bowel obstruction.
During operative repair of the
incarcerated hernia, there is no
evidence of strangulation

A. Cardiogenic shock due to

extrinsic causes
B. Cardiogenic shock due to
intrinsic causes
C. Hypovolemic shock
secondary to blood loss
D. Hypovolemic shock
secondary to third space
losses
E. Hypovolemic shock
secondary to insensible
losses
F. Septic shock
G. Neurogenic shock

4. A 25-year-old man is admitted to the

neurosurgery intensive care unit after a
motor vehicle accident. On admission
the patient is noted to have a blood
pressure of 120/80 mm Hg with a heart
rate of 105 beats/min. Upon evaluation
he is found to have a complete spinal
cord injury at the sixth cervical
vertebrae, as well as a bruise on his
abdomen in the distribution of his
seatbelt and a bruise on his chest from
hitting the steering wheel. Six hours
after admission the patient's blood
pressure gradually falls to 60/40 mm
Hg and the patient becomes
unresponsive.

A. Cardiogenic shock due to extrinsic

causes
B. Cardiogenic shock due to intrinsic
causes
C. Hypovolemic shock secondary to
blood loss
D. Hypovolemic shock secondary to
third space losses
E. Hypovolemic shock secondary to
insensible losses
F. Septic shock
G. Neurogenic shock

5. A 35-year-old man sustains a

50% full-thickness burn injury
to his torso and lower
extremities during a house
fire. Over the next 2 days, the
patient develops a worsening
paralytic ileus and a gradual
decrease in his blood pressure
to 80/60 mm Hg despite
following the Parkland formula
for determining the amount of
fluid to give after a burn
injury.

A. Cardiogenic shock due to extrinsic

causes
B. Cardiogenic shock due to intrinsic
causes
C. Hypovolemic shock secondary to
blood loss
D. Hypovolemic shock secondary to
third space losses
E. Hypovolemic shock secondary to
insensible losses
F. Septic shock
G. Neurogenic shock

6.During placement of a
triple lumen catheter in
a 72-year-old woman,
the patient suddenly
becomes hypotensive
with a blood pressure of
60/30 mm Hg during
advancement of the
guidewire.

A. Cardiogenic shock due to extrinsic

causes
B. Cardiogenic shock due to intrinsic
causes
C. Hypovolemic shock secondary to
blood loss

D. Hypovolemic shock secondary to

third space losses
E. Hypovolemic shock secondary to
insensible losses
F. Septic shock
G. Neurogenic shock

7. A 65-year-old, otherwise
healthy man underwent
laparoscopic cholecystectomy
3 weeks ago for acute
cholecystitis and cholelithiasis.
Now he presents with fever,
chills, and right upper quadrant
(RUQ) pain, and a new onset of
confusion, according to his
wife. He is tachycardic (130
beats/min), he appears flushed,
and his skin is warm

PHYSIOLOGIC RESPONSES

Neuroendocrine/inflammatory
maintain perfusion in cerebral and
coronary circulation

Persistent hypoperfusion
Hemodynamic derangement
End organ dysfunction/failure
Cell death

patient death

CLASSIFICATION
Hypovolemic

Traumatic
Septic (Vasogenic)
Cardiogenic
Obstructive

Neurogenic

Shock States & Haemodynamic Manifestations

Type

HeartRate

Stroke
Volume

CVP

PCWP

CO/CI

Pulse Rate

Hypovolemic

Spinal Shock

Anaphylaxis

Sepsis

Heart Block

Pump Failure

Relatively low

Relatively low

Volume Overload

Inflow obstruction

Outflow obstruction

Distributive

Cardiogenic

CAUSES
intravascular volume depletion hemorrhage
plasma volume extravascular sequestration
ascites
peritonitis

GI,GU, insensible losses

intestinal obstruction
heat

Hypoperfusion
blood volume
cardiac output

peripheral vasoconstriction
(compensatory)

DIAGNOSIS
The clinical signs of shock

Agitation
cool clammy
extremities
tachycardia,
weak or absent peripheral
pulses
hypotension.

HYPOVOLEMIC SHOCK

Classification of hemorrhage

THE APPROPRIATE PRIORITIES

ARE:
secure the airway,
IV volume resuscitation.
control the source of blood loss

TREATMENT (General)
REPLACE LOST VOLUME
STOP BLEEDING
VASOPRESSORS - ? Inotropic
support
AORTIC CROSS CLAMPING
Thermal Blanket
Pneumatic Anti-Shock Garment

PASG

PASG
1) Increase peripheral vascular
resistance by pressurizing the
arteries of the lower abdomen and
extremities.
2) Reduce the vascular volume by
compressing venous vessels.
3) Increase the central circulating
blood volume with blood returned
from areas under the garment.

4) Immobilize the lower extremities

and the pelvic region.

Fluid resuscitation
IV INFUSION

crystalloids continue to be
the mainstay of fluid choice.

hypertonic saline as a
resuscitative adjunct in
bleeding patients.

HYPERTONIC SALINE

BENEFITS OF HYPERTONIC SALINE

SOLUTIONS

Decreased reperfusion-mediated
injury
less impairment of immune
function
less brain swelling in the multiinjured patient
decrease in the incidence of ARDS
and multiple organ failure.

FLUID REPLACEMENT
In severe hemorrhage, restoration of
intravascular volume should be
achieved with blood products
packed red blood cells
Fresh frozen plasma (FFP)
Platelets
fibrinogen concentrate of
cryoprecipitate

TREATMENT
Too little volume allowing
persistent severe hypotension
and hypoperfusion is dangerous
too vigorous of a volume
resuscitation may be just as
deleterious.

Hypovolemic Shock
soft tissue injury, long bone
fractures
Pro- inflammatory mediator
systems (similar to Sepsis)
higher incidence of ARDS/
MOFS

second hit phenomenon

prompt control of hemorrhage

adequate volume resuscitation to
correct O2 debt
dbridement of nonviable tissue,
stabilization of bony injuries,
and appropriate treatment of soft
tissue injuries.

dysfunction of the endothelium

and vasculature secondary to
circulating inflammatory
mediators and cells

or as a response to prolonged
and severe hypoperfusion
failure of the vascular smooth

muscle to constrict
appropriately

Causes of Septic and Vasodilatory

Shock

Systemic response to infection

Noninfectious systemic
inflammation

Pancreatitis
Burns
Anaphylaxis
Acute adrenal insufficiency

 Prolonged, severe hypotension

Hemorrhagic shock
Cardiogenic shock
Cardiopulmonary bypass
Metabolic

Hypoxic lactic acidosis

Carbon monoxide poisoning

Host response to systemic

infection
Warm shock (hyperdynamic)
inflammatory

severe vasodilatation
peripheral resistance

hypodynamic (cold) - gross

decompensation

Findings include :
enhanced cardiac output

Peripheral vasodilation
fever
leukocytosis
hyperglycemia
and tachycardia

To quantify the magnitude of the

systemic inflammatory reaction
sepsis

Severe sepsis
septic shock

fever, tachycardia, and

tachypnea
Signs of hypoperfusion
confusion
malaise
oliguria
hypotension

insulin therapy
ventilatory support
IV infusion of recombinant
human activated protein
corticosteroids

Intrinsic
Compressive
pump failure

normal circulating volume

no change in peripheral
resistance

 hypotension
cool and mottled skin
depressed mental status
tachycardia
diminished pulses
dysrhythmia
precordial heave
distal heart tones

 electrocardiogram
urgent echocardiography.
chest radiograph
arterial blood gases

electrolytes
complete blood count
and cardiac enzymes

 support of the circulation

Intubation and mechanical ventilation
avoid fluid overload
Correction of electrolyte abnormalities
Pain control
Antiarrhythmic drugs, pacing, or
cardioversion

inotropic support
intra-aortic balloon pump.

Pericardial tamponade
Pulmonary embolus
Tension pneumothorax

Causes:
IVC obstruction
Deep venous thrombosis
Gravid uterus on IVC
Neoplasm

Increased intrathoracic pressure

Excess positive end-expiratory pressure
Neoplasm

Beck's triad consists of

hypotension,

muffled heart tones, and

neck vein distension

 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

 Ablation of vascular
sympathetic tone
venous capacitance, peripheral
resistance

hypoperfusion is minimal,
sequela infrequent
Pitfall - undetected
concomitant hypovolemia

Causes Spinal cord trauma

Spinal cord neoplasm
Spinal/epidural anesthetic

DIAGNOSIS
decreased blood pressure associated with
bradycardia (absence of reflexive tachycardia due
to disrupted sympathetic discharge)
warm extremities (loss of peripheral
vasoconstriction)

motor and sensory deficits indicative of a spinal

cord injury
and radiographic evidence of a vertebral column
fracture

TREATMENT
restoration of intravascular volume
alone
administration of vasoconstrictors

 Systemic/global
Lactate
Base deficit
Cardiac output

Oxygen delivery and consumption

Tissue specific
Gastric tonometry

Tissue pH, oxygen, carbon dioxide levels

Near infrared spectroscopy

Cellular
Membrane potential

Adenosine triphosphate