Pathology & Therapeutics II:

Review and Shock

Week 1

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 Pathophysiology Framework- Review
• Do you
• Etiologic factors
• Risk factors remember
Etiol
ogy what these
terms mean?
• Mechanism of disease/illness
Path
• Manifestations and complications
ologi
• S & S, body responses
• Can you give
cal
proc an example
ess
for each?
• Diagnostic Tests
Inter • Therapeutic Interventions
venti
ons

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Circulatory Failure
(AKA SHOCK)

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 Review
• What is cardiac output? (CO)

• What is mean arterial pressure? (MAP)

• What is systemic/peripheral vascular resistance

(SVR/PVR)?

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 Circulatory failure (Shock)
• A condition in which tissue perfusion is inadequate to deliver
oxygen and nutrients to support vital organs and cellular
function
• Result of life-threatening conditions or trauma
• The body attempts to compensate for inadequate perfusion
(homeostasis)
• What are the consequences of inadequate blood flow to
tissues?

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 Pathophysiology of Shock- Do you
remember the
Cellular Level Effects key differences
between
aerobic and
Metabolism changes to anaerobic due to anaerobic
hypoperfusion . metabolism?

ATP product is affected. What by-product

is also produced? How does this affect
the cell?

Na-K pump becomes impaired. What

effect will this have?

Cells are injured . What is released?

Cell death occurs.
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 Pathophysiology of Shock-
Compensation Mechanisms
• Goal: Maintain BP and CO You learned
about how the
SNS and RAA
• 2 Key Mechanisms:
work in anatomy
1. Sympathetic nervous system class.
• What is the role of the SNS? Now it is time to
• What is released? apply it!
• How will it help in shock?

2. Renin-angiotensin-aldosterone mechanism
• What is the effect of this mechanism?
• How will it help in shock?

• Other compensation mechanisms exist but have smaller effects on shock

• Overtime, compensation mechanism can lead to further deterioration.
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 Compensatory Mechanisms in Shock

What are the

other
compensatory
mechanisms?

SNS

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Fig 20-8- p503 Compensatory
Mechanisms

Attempts to Maintain
Circulatory Function and
Blood Volume

Think about the SNS vs. RAA

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 Stages of Shock
Compensatory Progressive Irreversible
Patho Compensation Compensation Hypoperfusion
mechanisms initiated mechanisms can’t keep severely damages
in response to low up, hypoperfusion multiple organs
perfusion worsens, cell damage
Key • BP normal • BP ↓ • BP ↓↓↓
Effects • HR ↑ • HR ↑↑ • Metabolic acidosis
• Cool clammy skin • Cardiac ischemia worsens
• Decreased bowel • dysrhythmias • Multiple organs fail
sounds • Urine output ↓↓
• Urine output ↓ or absent
• Blood glucose ↑ • Hypoxia, pulmonary
• RR ↑ edema
• Metabolic acidosis • Decreased LOC
• Anxious or confused • Altered liver, GI,
hematological etc.
Prognosis Good with early Worsens- Depends on Does not respond to
intervention and time to restore treatment … Death
correction of cause perfusion, damage etc.

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 Types of Shock (Overview)

Cardiogenic Hypovolemic Obstructive Distributive

Change in
blood flow
due to
Alteration in Decrease in Obstruction increased
cardiac blood of blood vasodilation
function volume flow • Anaphylactic
• Neurogenic
• Septic

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 Hypovolemic Shock
• Caused by diminished blood volume with decreased filling of
the circulatory system

Caused by loss of:

– Whole blood
• hemorrhage, internal bleeding
– Plasma
• severe burns
– Extracellular fluid
• GI losses from vomiting & diarrhea, third-spacing

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Pathophysiology of Hypovolemic Shock

What
compensatory
mechanisms
will be
initiated?

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Identify the Manifestations of Hypovolemic
Shock
• Early Signs: • Late Signs:

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 Hypovolemic Shock Treatment
• Correct or control
underlying problem
• Reestablish vascular
volume
– IV fluid, blood products
• Positioning
• Oxygen
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• Medications (vasoactive)
• may be needed to increase
BP AFTER blood volume
deficit has been corrected to
help improve blood flow to
kidneys and other organs
• Ongoing assessment &
monitoring
15
 Cardiogenic Shock
• Heart fails to pump blood adequately

• Causes are coronary and non-coronary in origin:

– Damage to heart (MI)
– Ineffective pumping (arrhythmias)
– Mechanical defects (i.e. septal damage, valve damage)
– Post-cardiac surgery complications
– End-stage cardiac conditions (i.e. CAD, cardiomyopathy)

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Pathophysiology of Cardiogenic Shock

** Don’t forget
about the
compensatory
mechanisms…

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 Think about it…
• Decreased cardiac output & lowers BP
– Effect on contractility? Preload? Afterload?

– Hypoperfusion despite normal volume

• Sympathetic system responds

– Vasoconstriction increases resistance to blood flow.

• RAA is activated. Effects?

• Increased workload on heart worsens heart failure

and affects coronary perfusion.
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Manifestations of Cardiogenic Shock
• Dysrhythmias • Think about it…
• Hemodynamic instability What is the
– MAP and BP decrease pathophysiology
– Decreased urine output causing these
• Similar appearances to heart manifestations?
failure
– Cyanosis of lips, nail bed & skin
– Pulmonary edema
• Changes in LOC

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 Treatment of Cardiogenic Shock

• Key goals:
– Limit further myocardial
damage and protect Improve CO
healthy myocardium

 workload  coronary
and O2 needs perfusion

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 Treatment of Cardiogenic Shock
• Oxygen and pain control
• Hemodynamic monitoring
• Don’t forget to treat
Medications (vasoactive)
the cause of the
• Fluid therapy cardiogenic shock…
• Mechanical assistive
devices (IABP)

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 Obstructive Shock
• Due to mechanical impediment to
flow of blood through central
circulation (great veins, heart, & pulmonary
circulation).

• Caused by:
• Dissecting aortic aneurysm
• Cardiac tamponade
• Pneumothorax
• Pulmonary embolism (most common)

• Creates increased pressure within

the right side of heart What will
– This leads to decreased blood return to happen to the
heart CO?
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 Obstructive Shock

• Symptoms of right sided heart failure develop

• Treatment focus on reversing underlying cause

– Examples?

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 Distributive Shock
• Occurs when blood volume is
abnormally displaced in the
vasculature away from the
heart and central circulation

Further classified into 3 types:

1. Neurogenic shock
2. Anaphylactic shock
3. Septic shock
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Pathophysiology of Distributive Shock

Compensatory
mechanisms are
either impaired or
unable to
overcome the
effects of
distributive shock

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 Neurogenic Shock
• Caused by vasodilation resulting
from loss of sympathetic tone

• Can result from

– spinal cord injury
– spinal anesthesia
– nervous system damage
– lack of glucose

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 Neurogenic Shock
Interrupted SNS signals to blood vessels,
baroreceptors and thermoregulation system

Relaxation of smooth muscle in blood vessel

walls

Decreased systemic/peripheral vascular

resistance (massive vasodilation)

Result- hypotension, decreased CO,

bradycardia
Leading to: impaired peripheral perfusion
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 Neurogenic Shock
• Transient
– Onset in minutes, duration up to 3 weeks

• Key Symptoms:
– Bradycardia (baroreceptors cannot increase HR)
– Hypotension (vasodilation, decreased CO)
– Warm flushed skin
– Piokilothermy (loss of SNS thermoregulation ability)

• Key treatments:
– Restore BP with: IV fluids, vasoactive medications
– Restore HR -Medication to increase HR (i.e.. atropine)
– Restore Temp-Warming/cooling
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blankets if need 28
 Anaphylactic Shock
• Occurs rapidly & is life-threatening

• Caused by severe allergic reaction

– May occur with one exposure or after several exposures to an
antigen
– Involves an antigen-antibody reaction
• Mast cells release Histamine which causes widespread vasodilation,
increased capillary permeability

• Most common triggers :

– Medication reactions (i.e.. penicillin) What will
– Foods (nuts, shellfish) happen to the
CO and SVR?
– Insect venom (bee stings)
– Latex allergy PATH 1017 20/21 29
Anaphylactic Shock Manifestations:
• Anxiety
• Laryngeal edema (life-threatening)
• Bronchospasm
• Hypotension
• Tachycardia, weak pulse
• Pruritis (itching)
• Angioedema
• Urticaria (hives)
• Abdominal cramps (GI & uterine smooth muscle contraction)
• Loss of consciousness (late)

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 Anaphylactic Shock Treatment

– Remove triggering agent immediately

– ABCs
– Fluids
– Drugs:
– Epinephrine (i.e.. Epi-Pen)
– Antihistamines (benadryl), corticosteroids
– Vasoactive drugs
– Bronchodilators
– Intubation & oxygen may be needed
– Prevention is best!

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 Septic Shock
• Most common type of distributive shock

• Most commonly caused by gram-negative bacteria

– Bacteremia and pneumonia common precursors

• Elderly patients at particular risk

• Prognosis: 28-50% die

• Prevention important
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 Septic Shock
Microorganism invade tissues and triggers immune
response

Massive release of biochemical and inflammatory

mediators (i.e.. cytokines etc.)

Systemic inflammatory response occurs

What will
Leads to massive increase in capillary permeability happen to
and vasodilation the CO
and SVR?

Result: inadequate perfusion, oxygenation and

nutrients to tissues eventually organ dysfunction
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 Septic Shock- 2 Phases
• High CO
• Vasodilation (SVR)
Warm Phase • BP normal; HR ; RR 
(hyperdynamic, • Fever, warm & flushed skin
progressive) • May have  urine output;  bowel
sounds; confusion/agitation

• Low CO
• Vasoconstriction (cool, pale skin)
Cold Phase • temp;  HR;  RR
(hypodynamic, • Anuria
irreversible) • Leads to organ failure, death

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 Septic Shock Treatment

• Identify cause (i.e.. C&S) and treat cause if possible

• Fluid replacement
• Oxygen (may require mechanical ventilation if shock is progressing)

• Pharmacological:
• Antibiotics
• Vasoactive drugs
• Antipyretics
• Corticosteroids

• Other aspects of treatment;

– Nutritional support
– Control blood glucose levels (insulin tx)

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 Complications of Shock
Acute respiratory distress • Rapid onset of severe dyspnea
syndrome • Accumulation of neutrophils in alveoli

• Vasoconstriction causes renal tubule

Acute renal failure
ischemia/ATN

Gastrointestinal • Ischemia to GI tract  ulcers

complications • Decrease in mucosal perfusion

Disseminated intravascular • Microinfarcts, ischemia

coagulation (DIC) • Bleeding problems

Multiple organ dysfunction • Altered organ function such that homeostasis

syndrome (MODS) cannot be maintained without intervention

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