SHOCK

PHYSIOLOGY OF BLOOD
PRESSURE

Summary of factors that increase

blood pressure:

Mechanism of increase cardiac

output
There are 2 mechanism to increase cardiac
output:
Instrinsic cardiac regulation
Extrinsic cardiac regulation

Extrinsic Regulation of Heart

Pumping
1.
2.
3.
4.

Autonomic Nervous System

Hormone
Chemical Substance
Temperature

1. 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

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

ADH / Vasopressin

3. 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

4. Temperature
Increased body temperature
Increases HR
Decreased body temperature
Decreases HR

SHOCK

DEFINITION
o Shock is

a condition in which the cardiovascular

system fails to perfuse tissues adequately
oAn impaired cardiac pump, circulatory system,
and/or volume can lead to compromised blood
flow to tissues
oInadequate tissue perfusion can result in:
generalized cellular hypoxia (starvation)
widespread impairment of cellular metabolism
tissue damage
death

organ failure

Classification of Shock

1. Hypovolemic shock
the most common type loss of circulating blood
volume. loss of whole blood, plasma, interstitial
fluid , or a combination.
2. Cardiogenic shock
failure of the heart as a pump, as in arrhythmias or
acute myocardial infarction (MI).

3. Vasogenic shock decreased resistance within

capacitance vessels, usually seen in sepsis.
3.a. Neurogenic shock
is a form of vasogenic shock in which spinal cord
injury or spinal anesthesia causes vasodilation due
to acute loss of sympathetic vascular tone.

5. Obstructive shock (cardiogenic shock)

results from mechanical impediment to circulation
leading to depressed cardiac output. such as
pulmonary embolism or tension pneumothorax.
6. Traumatic shock
soft tissue and bony injury lead to the activation of
inflammatory cells and the release of circulating
factors, such as cytokines and intracellular
molecules that modulate the immune response.

PATHOPHYSIOLOGY OF SHOCK

Stages of Shock
Initial stage

tissues are under perfused

decreased CO
increased anaerobic metabolism
lactic acid is building
Hypoperfusion causes hypoxia. Due to the lack of
oxygen, the cells perform lactic acid fermentation.
Accumulating pyruvate is converted to lactate by
lactate dehydrogenase
causing lactic
acidosis.

Compensatory stage
Reversible
SNS activated by low CO attempting to
compensate for the decrease tissue perfusion.

Progressive stage
Positive Feedback Shock becomes more progressive
Cardiac Depression : coronary blood flow decreases
below that required for adequate nutrition of the
myocardium
Vasomotor failure : diminished blood flow to the brains
vasomotor center depresses the center so much and
become less active
Sludged blood : blockage in small vessels because
tissues metabolism product
Increased Capillary Permeability : Capillary hypoxia lead
to increases capillary permeability. Large quantity of
fluid transudes
Release of toxins by ischemic tissue : serotonin,
histamine, tissue enzymes

Irreversible or refractory stage

The vital organs have failed and the shock can

no longer be reversed. Brain damage and cell

death are occurring, and death will occur
imminently.
One of the reasons that shock is irreversible at

this point is that much cellular ATP has been

degraded into adenosine in the absence of
oxygen as an electron receptor in the
mitochondrial matrix. Adenosine easil perfuses
out of cellular membranes into extracellular
fluid, furthering capillary vasodilation, and then
is transformed into uric acid.

Clinical Presentation
Vital signs
Hypotensive: < 90 mmHg
MAP < 60 mmHg
Tachycardia: Weak and Thready pulse
Tachypneic

Clinical Presentation
Mental status
restless, irritable, apprehensive
unresponsive, painful stimuli only

Decreased Urine output

Hypovolemic Shock
Loss of circulating volume Empty tank
decrease tissue perfusion
response

general shock

ETIOLOGY:

Internal or External fluid loss

Intracellular and extracellular compartments

Most common causes:

Hemmorhage
Dehydration

Hypovolemic Shock: External loss of fluid

Fluid loss: Dehydration
Nausea & vomiting, diarrhea, massive diuresis, extensive
burns
Blood loss:
trauma: blunt and penetrating

Hypovolemic Shock:

Internal fluid loss

Loss of Intravascular integrity

Increased capillary membrane permeability
Decreased Colloidal Osmotic Pressure

Management Hypovolemic Shock

Ensure adequate oxygenation (ABC)
Treat Underlying Cause (Ex : Provide control of

hemorrhage)
Give Fluid Resuscitation
Isotonic Crystalloid solution (10-20 mL/kg)
Administer PRC if patients have heavy bleeding

or unresponsive to fluid resuscitation.

Blood Transfusion
Hb < 8gr%
Ht < 30%
In adult with lung or heart abnormality Hb<10
g/dl
Major surgery blood loss >20% blood volume

1 unit packed red cell Hb >1 gr% &

hematocrit > 2 - 3%.
PRC 10 ml/kgbb Hb 3 gr%

Cardiogenic Shock
The impaired ability of the heart to pump

blood
Common cause :
Acute myocardial infarction
Severe myocarditis
Cardiomyopathy
Most common cause is LV MI (Anterior)

Highest mortality rate

Characteristic:
Low cardiac output
Cardiac filling pressure
Systemic Vascular Resistance

Management
Focus on improve myocardial contractility and pump

function
Establish or maintain airways if needed give
mechanical ventilation decrease work of breathing
Give Vasopressor or Inotropic drugs, if Hypovolemia
present correct with crystalloid or blood product
before administering
Norepinephrine (0,5 mcg/min)
Dobutamine (5 mcg/kg/min)
Treat underlying disease
Myocardial Infarction : Acetylsalicylic Acid /
Fibrinolytic agents.
Arrthymia : give antiarrthymic drug

Obstructive Shock
Resulted from impediment to normal flow of blood,

either due to obstruction to the outflow of blood

from the heart, or increase resistance to cardiac
filling during diastole
Common Cause :
Pulmonary embolism
Aortic stenosis
Cardiac tamponade
Tension pneumothorax

Characteristics :
Low cardiac output
Cardiac filling pressure
Systemic Vascular Resistance

Management
Pericardial tamponade
pericardiocentesis
surgical drainage
Pulmonary embolism
heparin
ventilation/perfusion lung scan
pulmonary angiography
thrombolytic therapy & embolectomy at surgery

Distributive Shock
Common cause :
Septic shock
Anaphylactic shock
Neurogenic shock
Characteristics :
Normal or high cardiac output
Systemic vascular resistance
Cardiac filling pressure

Anaphylactic shock
A type of distributive shock that results from

widespread systemic allergic reaction to an

antigen
Pathophysiology :
Antigen exposure

Body stimulated to produce IgE antibodies

specific to antigen (drugs, bites, contrast,
foods, vaccines)
Reexposure to antigen : IgE binds to mast
cells and basophils

Managemenet
airway support
iv epinephrine
antihistamines : diphenhydramine 50 mg iv
corticosteroids
Prevention : Patient education

Neurogenic shock
A type of distributive shock that results from

the loss or suppression of sympathetic tone

Causes massive vasodilatation in the venous
vasculature, venous return to heart,
cardiac output.
Most common etiology: Spinal cord injury
above T6

Management
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

Septic Shock
Sepsis : Systemic Inflammatory Response (SIRS)

to infection manifested by 2 or > of following:

Temp > 38 or < 36
HR > 90
RR > 20 or PaCO2 < 32
WBC > 12,000/cu mm or > 10% Bands (immature

wbc)

Septic shock :

Sepsis with:
Hypotension (SBP < 90)
Tissue perfusion abnormalities invasion of the
body by microorganisms & failure of bodys
defense mechanism.

Management
Identify site of infection and drain
Antimicrobial agents
Monitoring and support with fluids,

vasopressors, and inotropic agents

In summary, Treatment of Shock

Identify the patient at high risk for shock
Control or eliminate the cause
Implement measures to enhance tissue

perfusion
Correct acid base imbalance
Treat cardiac dysrhythmias

THANK