SHOCK

DEFINITION
unable to provide adequate circulation to the vital
body organs due to hemodynamic and metabolic
disorders.

Mechanical Requirements for Adequate Tissue Perfusion:

o Fluid
o Pump
o Vessels
Pressure generated/ Blood pressure is a rough measurement
of tissue perfusion.
The pressure is depend on cardiac output (CO) and systemic
vascular resistance (SVR)

PHYSIOLOGY OF
BLOOD PRESSURE

MECHANISM OF INCREASE
CARDIAC OUTPUT
There are 2 mechanism to increase cardiac output:
Instrinsic cardiac regulation
Extrinsic cardiac regulation

INTRINSIC CARDIAC
REGULATION

EKSTRINSIC CARDIAC
REGULATION
1.
2.
3.

Autonomic Nervous System

Hormone
Chemical Substance

4.

Temperature

AUTONOMIC
NERVOUS SYSTEM
Sympathetic (Cardiac Accelerator)
Increases Heart Rate (HR)
Increases the force of heart contraction
Increases the conduction of impulses from the atria to the
ventricles
* Inhibition : decrease cardiac pumping
Parasympathetic (Vagus) (Cardiac Inhibitor)
Decreases HR
Slight decrease in heart contraction
Decreases the conduction of impulses from the atria to the
ventricles

HORMONES
Thyroid
Increases metabolism vasodilation increases blood flow
increases Stroke Volume
(Increases CO)
Increases HR
Epinephrine and Norepinephrine
Sympathomimetic

CHEMICAL
SUBSTANCES
Kalium [K+]
: decreases HR, block conduction, weaker contraction
: increases HR
Calcium [Ca2+]
: stronger contraction
: weaker contraction
Natrium [Na+] : weaker contraction
CO2 / pH
Low pH : increasing sympathetic signal (venous return )
O2
Low O2 : vasoconstriction

TEMPERATURE
Increased body temperature
Increases HR
Decreased body temperature
Decreases HR

TYPES OF SHOCK
Hypovolemic shock
o Blood volume problem
Cardiogenic shock
o Blood pump problem
Distributive shock
o Blood vessel problem
- Neurogenic shock
- Septic shock
- Anaphylactic shock

PATHOPHYSIOLOGY
OF SHOCK
Impaired tissue perfusion occurs when an imbalance
develops between cellular oxygen supply and cellular
oxygen demand.
All Types of shock eventually result in impaired tissue
perfusion & the development of acute circulatory failure or
shock syndrome.

Cells
Cells switch
switch from
from aerobic to anaerobic metabolism

lactic
lactic acid
acid production
production

Cell
Cell function
function ceases
ceases & swells
swells

membrane
membrane becomes
becomes more
more permeable
permeable

electrolytes
electrolytes &
& fluids
fluids seep in & out of cell

Na+/K+
Na+/K+ pump
pump impaired
impaired

mitochondria
mitochondria damage
damage
cell
cell death
death

COMPENSATORY MECHANISM
SYMPATHETICNERVOUS SYSTEM (CNS) ADRENAL
RESPONSE
SNS Neurohormonal response Stimulated by baroreceptor
Increased heart rate
Increased contractility
Vasoconstriction (afterload)
Increased preload

SNS Hormonal : RAA system

Decrease renal perfusion
Activated RAA system
Angiotension II potent vasoconstriction & releases aldosterone
adrenal cortex sodium & water retention ( intravascular
volume)

SNS Hormonal : antiduiretic hormone

Osmoreceptors in hypothalamus stimulated
ADH released by posterior pituitary gland vasopressor effect to
increase BP acts on renal tubules to retain water

SNS hormonal: Adrenal cortex

Anterior pituitary releases adrenocorticotropic hormone
(ACTH)
Stimulates adrenal cortex to release glucocorticoids
Blood sugar increases to meet increased metabolic needs

FAILURE OF
COMPENSATORY RESPONSE
Decreased blood flow to the tissues causes cellular hypoxia
Anaerobic metabolism begins
Cell swelling, mitochondrial disruption, and eventual cell
death
If low perfusion states persists:
IRREVERSIBLE DEATH IMMINENT

STAGES OF SHOCK
Initial stage
Tissue are under perfused, decreased CO, increased
anaerobic metabolism, lactic acid is building
Compensatory stage
Reversible. SNS activated by low CO, attempting to
compensate for the decrease tissue perfusion.

Progressive stage
Falling compensatory mechanism: profound
vasoconstriction from the SNS ischemia lactic acid
production is high metabolic acidosis
Irreversible or refractory stage
Cellular necrosis and multiple organ dsyfunction syndrome
may occur
Death Is Imminent

CLINICAL
PRESENTATION
Vital signs
Hypotensive <90mmHg, MAP <60mmHg, tachycardia (weak
and thready pulse), tachypneic
Mental status
Restless, irritable, apprehensive, unresponsive, painful stimuli
only
Decreased urine output

HYPOVOLEMIA
SHOCK

HYPOVOLEMIA
SHOCK
Loss of circulating volume (Empty tank)
Result decrease of tissue perfusion general shock
response
Etiology :
Internal or External fluid loss
Intracellular and extracellular compartments
Most common causes :
Haemorrhage
Dehydration
Hypovolemic Shock is a relatively common complication of
severe hemorrhage and/ or fluid loss in surgcal patients

EXTERNAL LOSS OF FLUID

Fluid Loss :
(Dehydration)
Nausea & vomitting
Diarrhea
Massive diuresis
Extensive burns

Blood Loss :
Trauma (blund &
penetrating)
*BLOOD YOU SEE
*BLOOD YOU
DONT SEE

INTERNAL FLUID
LOSS
Loss of Intravascular integrity
Increased capillary membrane permeability
Decreased coloidal Osmotic Pressure (third spacing)

PATHOPHYSIOLOGY
Decreased intravascular volume
Decreased venous return (preload, RAP)
Decreased ventricular filling (preload, PAWP)
Decreased stroke volume (HR, preload, and afterload)
Decreased CO
Inadequate tissue perfussion

MANAGEMENT
HYPOVOLEMIC SHOCK
Secure airway, establish two large-bore Ivs (and possibly a
central line), and administer supplemental O2
Volume resuscitation
- Rapid infusion of IV fluids (normal sakine or LR). Infuse 2L or
3 times the amount of estimated blood loss (no evidence has
proven albumin/ colloid solutions to be beneficial)
- Emergent RBC transfusion for hemorrhage

Inotropic support (only used afterv replacing volume)

- Dopamine if hypotensive (inotropy plus vasoconstriction)
- Dobutamine if normotensive (inotropy plus vasodilatation)
- In general, avoid vasocontrictiors as they will increase BP via
vasocontriction but may not improve perfusion
Replace electrolytes as necessary
Clotting factors: give fresh frozen plasma and platelets for
every 5 units of blood infused
Surgery to identify and repair the sites of uncontrolled
bleeding

CARDIOGENIC
SHOCK

CARDIOGENIC SHOCK
Cardiogenic shock is the impaired ability of the heart to
pump blood. Pump failure of the right or left ventricle.

PRESENTATION
Systolic
Systolic BP
BP <90mmHg
<90mmHg
Pulse
Pulse pressure
pressure <20
<20
Cyanosis,
Cyanosis, ashen
ashen skin
skin color,
color,
diaphoresis,
diaphoresis, mottled
mottled extremities
extremities
Altered
Altered mental
mental status
status
Tachycardia
Tachycardia
Tachypnea
Tachypnea
Dyspnea
Dyspnea
Waek
Waek distal
distal puses,
puses, cool
cool extremties
extremties
Crackles
Crackles in
in lungs
lungs
oliguria
oliguria

TREATMENT
Airway control with intubation.
Fluid resuscitation as necessary to maximize cardiac filling
and output.
IV inotrope administration
- Dopamine ( and agonist) for hypotensive patients to
cause increased inotropy and vasoconstriction.
- Dobutamine ( agonist only) for normotensive patients to
cause increased inotropy and vasodilatation

Avoid vasopressors (e.g., neosynephrine, norepinephrine) as

they may improve blood pressure, but may diminish tissue
perfusion
Correct arrhythmias immediately with cardioversion, external
pacing, and medications.
PTCA is the preferred method for reperfusion in cases of
cardiogenic shock following MI; thrombolytics are much less
effective in shock states.

Correct electrolyte abnormalities as necessary.

Intra-aortic baloon pump placement may be used as a
temporizing measure to decrease afterload, thereby
improving perfusion and cardiac output.

VASOGENIC/
DISTRIBUTIVE
SHOCK

VASOGENIC /
DISTRIBUTIVE SHOCK
Neurogenic
Shock
Septic Shock
Anaphylactic
Shock

NEUROGENIC
SHOCK

NEUROGENIC SHOCK
A type of distributive shock that results
from the loss or suppression of
sympathetic tone
Most common etiology: Spinal cord injury
above T6
Loss of sympathetic tone
Neurogenic is the rarest form of shock!
massive vasodilatation in the venous vasculature
Decrease venous return to heart
Decrease cardiac output

Distruption of sympathetic nervous system

Loss of sympathetic tone
PATHOPHYSIOLOGY
Venous and arterial vasodilation
Decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased cellular oxygen supply
Impaired tissue perfusion
Impaired cellular metabolism

ASSESEMENT

MANAGEMENT
Goals of Therapy are to treat or remove the
cause & prevent cardiovascular instability, &
promote optimal tissue perfusion
Secure airway, establish two large-bore IVs
(and possibly a central line), and administer
supplemental O2
Administer large fluid volumes of normal
saline or lactated ringers solution to
compensate for the increased intravascular
space

Maintain C-spine protection

Rapid fluid administration is generally successful in the
absence of other interventions
Atropin and/or cardiac pacing for significant bradicardia
Methylprednisolone IV bolus and infusion in cases of blunt
spinal cord injury.

Vasopresor drips
Alpha agonist to augment tone if perfusion still
inadequate
dopamine at alpha doses (> 10 mcg/kg per min)
ephedrine (12.5-25 mg IV every 3-4 hour)

Treat bradycardia with atropine 0.5-1 mg doses

to maximum 3 mg
may need transcutaneous or transvenous pacing
temporarily

SEPTIC
SHOCK

SEPSIS
Systemic Inflammatory Response (SIRS) to INFECTION
manifested by two or > of following:

Temp > 38 or < 36 centigrade

HR > 90

RR > 20 or PaCO2 < 32

WBC > 12,000/cu mm or > 10% Bands (immature

wbc)

SEPTIC SHOCK
SEPSIS WITH:
Hypotension (SBP < 90 or > 40 reduction from baseline) &
Tissue perfusion abnormalities invasion of the body by
microorganisms & failure of bodys defense mechanism.

RISK FACTOR ASSOCIATED

WITH SEPTIC SHOCK

PATHOPHYSIOLOGY
Initiated by gram-negative (most common) or gram positive bacteria,
fungi, or viruses
Cell walls of organisms contain Endotoxins
Endotoxins release inflammatory mediators (systemic inflammatory
response)
Vasodilation & increase capillary permeability leads to
Shock due to alteration in peripheral circulation & massive dilation

IMMUNE / INFLAMMATORY
RESPONSE
Microorganisms enter body

Mediator Release

Activation of Complement, kallikrein / kinin/ coagulation

& fibrinolytic factors platelets, neutrophils &
macrophages>>damage to endothelial cells.

ORGAN DYSFUNCTION

CLINICAL
PRESENTATION
Two phases:

Warm shock - early phase

hyperdynamic response,
VASODILATION
Cold shock - late phase
hypodynamic response
DECOMPENSATED STATE

CLINICAL
MANIFESTATION
EARLY STATE

L ATE STATE

(HYPERDINAMIC COMPENSATION)

( HYPODI NAM IC DECIM PENSATION)

Massive vasodilation
Pink, warm, flushed
skin
Increased Heart Rate
Full bounding pulse
Tachypnea
Decreased SVR*
Increased CO & CI
SVO2 will be
abnormally high
Crackles

Massive vasodilation
Pink, warm, flushed
skin
Increased Heart Rate
Full bounding pulse
Tachypnea
Decreased SVR*
Increased CO & CI
SVO2 will be
abnormally high
Crackles

MANAGEMENT
Prevention !!! Find and kill the source of the infection
(begin IV empiric antibiotics to cover likely
pathogens based on the presenting clinical picture)
Fluid Resuscitation
Vasoconstrictors
Inotropic drugs
Maximize O2 delivery Support
Nutritional Support
Comfort & Emotional support

SEQUELAE OF SEPTIC
SHOCK
The effects of the bacterias endotoxins can continue even
after the bacteria is dead!!!

ANAPHYLACTIC
SHOCK

ANAPHYLACTIC
SHOCK

A type of distributive shock that results from widespread systemic

allergic reaction to an antigen
Anaphylactic is a severe, systemic, immune-mediated allergic reaction
resulting in urticarial rash, respiratory distress due to upper and/or lower
airway obstruction, and vascular collapse due to vasodilation
Most commonly a type I hypersensitivity reaction (IgE-mediated)

COMMON CAUSES INCLUDE:

PRESENTATIONS
EARLY SYMPTOMPS

LATE SYMPTOMPS

Nasal congestion,
hoarseness
Dyspnea, wheezing,
cough
Skin flushing, severe
pruritus, urticaria
Chest pain/ tightness
Nausea/ vomiting,
abdominal cramping

Airway obstruction,
stridor, angioedema,
tongue/pharynxs
sweeling
Altered mental
status, seizure
Hypotension,
tachycardia,
dysrhythmias

TREATMENT
Establish IV access, high-flow O2, cardiac monitoring, pulse
oximetry
Assess airway early as swelling can rapidly cause airway
compromise.
- Endotracheal intubation if possible; however, swelling ay
prohibit intubation
- Surgical airway (jet insufflation or cricothyrotomy) may be
necessary

Rapidly administer IV fluids (2-4L of NSS or LR)

Epinheprine decreases airway edema, restores vascular tone
- IV epinephrine for severe bronchospasm, respiratory arrest,
refractory shock, or upper aorway obstruction.
- Subcutaneous administration for less severe symptoms

Antihistamines (IV diphenhydramine plus an H2 blocker) will

prevent further mast cell degranulation
Albuterol nebulizers to treat bronchospasm
Dopamine or norepinephrine may be used to maintain
vascular tone in patients with persistent hypotension.