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Module 11 - Shock and Multiple Organ Dysfunction Syndrome (MODS)

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Shock occurs when
occurs when cardiovas system can no longer provide adequate perfusion of nutrients and O2 to vital tissues.
The causes of shock
can be divided into those that primarily arise from cardiac dysfunction, loss of blood volume, or a failure to maintain an appropriate vasc resistance.
No matter what the cause of shock, the result is
underperfusion of vital tissues and impairment of cellular metabolism.
One of the primary insults to cells is a lack of adequate oxygen supply. When this occurs, cells shift to anaerobic metabolism, which results in:
1. A reduction in ATP

2. inability of the cells to maintain their normal membrane electrolyte pumps causing sodium, chloride, and calcium to accumulate in cells and cellular lysis
When cells become ischemic, the inflammatory response is activated, with release of numerous:
Cytokines
Lysosomal enzymes
Activators of the clotting cascade
Finally, anaerobic metabolism produces
lactic acid,
- which lowers the blood and tissue pH.

This further interferes with cellular metabolism and electrolyte balance.
If the shock state persists,
multiple organ dysfunction develops.
MODS
Another important cellular dysfunction associated with shock is impairment in the ability of cells to take up enough glucose to fuel cellular metabolism, which results in
all of the same problems just described with inadequate delivery of oxygen to cells.
Fortunately, systemic compensation for the shock state includes the
- release of cortisol,
- thyroid hormone, and
- catecholamines, which increase glucose production.
However, once glycogen stores are used up, gluconeogenesis is activated to
continue glucose production, but at the expense of protein depletion.
As proteins are broken down, they release alanine, which can contribute to lactic acid production as well as the release of ammonia and urea,
which are toxic to cellular metabolism.
Muscle dysfunction from protein degradation contributes to
multiple organ dysfunction.
Cardiogenic shock
Inability of the heart to generate an adequate CO
- ischemic heart disease
- cardiomyopathy
- dysrhytmias
- HF
- valve disease
- pericardial disease

RESULT - inability to perfuse organs
Hypovolemic shock
Lack of adequate blood volume
- DEHYDRATION
- diarrhea
- burns
- hemorrhage

RESULT - inability to perfuse organs
Distributive shock
Inability to maintain a normal peripheral vascular resistance
- anaphylaxis
- neurogenic (trauma, drugs, stroke)
- sepsis

inadequate peripheral resistance

RESULT - inability to perfuse organs
Cardiogenic Shock
can occur whenever the heart is unable to generate an adequate CO.

This state describes severe systolic heart failure and shares all of the same potential causes such as:
- myocardial infarction,
- cardiomyopathies,
- dysrhythmias,
- valvular diseases,
- and pericardial diseases.

When THIS shock occurs in the setting of acute myocardial infarction, mortality is greater than 70%.
Clinical Manifestations of cardiogenic shock - the signs and symptoms of:
- Pulmonary edema
- dyspnea,
- inspiratory crackles
- Severe underperfusion of vital organs
- poor capillary refill, cyanosis,
- cold clammy extremities,
- oliguria
Evaluation of cardiogenic shock Diagnosis is confirmed by measurement
of BP and electrolyte levels and with the use of echocardiography and venous or arterial catheterization.
Treatment of cardiogenic shock —Management includes the use of
pressors such as dobutamine,
- careful fluid management,
- and treatment of the underlying cardiac abnormality if possible.

Rapid intervention with restoration of coronary perfusion and the use of ventricular assist devices may allow some patients to survive until the acute condition has been stabilized.
Hypovolemic Shock
Any condition that can result in the loss of greater than 15% of the intravascular volume can cause hypovolemic shock.

These conditions include:
- Dehydration
- Overuse of diuretics or dialysis
- Hemorrhage
- Burns
- Extreme hyperglycemia or hypercalcemia
- Severe diarrhea
If the compensatory mechanisms such as
- activation of the renin-angiotensin-aldosterone system
- and antidiuretic hormone,
- increased heart rate,
- and increased peripheral vascular resistance

are inadequate to maintain tissue perfusion, then shock ensues.
Clinical manifestations
-Individuals with hypovolemic shock will develop all of the clinical manifestations of underperfusion of vital organs discussed under cardiogenic shock

but will not develop pulmonary edema.
Evaluation includes
- seeking the source of volume loss
- and measuring BP, hemoglobin, and electrolyte levels.
Management-Treatment consists of
reversing the underlying loss of fluid
(blood if indicated) and intravenous fluid administration
Distributive shock is a shock classification used to
describe the inability to maintain an adequate peripheral vascular resistance.

This type of shock occurs most commonly in neurogenic insults, anaphylaxis, and sepsis
Neurogenic shock occurs when
injury to the brain or spinal cord or the administration of certain drugs results in the loss of sympathetic stimulation.

It can also occur when pain, stress, drugs, or toxins cause overstimulation of the parasympathetic nerves.

Arterioles lose their stimulus to maintain a constant amount of vasoconstriction (loss of vascular tone) and, therefore, peripheral vascular resistance falls.

This causes the blood volume to be redistributed to nonvital organs, with a loss of blood pressure and underperfusion of tissues.
Clinical manifestations—Individuals in neurogenic shock will frequently present with
a very low peripheral vascular resistance and
bradycardia in the setting of neurogenic insult.
Management includes
- treatment of the underlying insult as well as
- careful patient positioning,
- the administration of pressors, and appropriate fluid management.
- Many individuals will recover adequate vascular tone over time if they survive the acute syndrome.
Anaphylactic shock occurs in
severe allergic reactions.

When an allergic individual is exposed to high doses of allergen, the immune reaction may be so severe that IgE is produced at very high levels.
resulting in:
- Widespread degranulation of mast cells, with release of multiple vasoactive and inflammatory mediators

- Profound peripheral vasodilation and increased capillary permeability

- Decrease in BP and tissue perfusion
Anaphylactic shock can be further exacerbated by
both upper and lower airway muscle spasms, with inability to ventilate and oxygenate, and by severe diarrhea with loss of blood volume.
Clinical manifestations—Individuals with anaphylactic shock will often present with a history of
- allergies and with urticaria,
- stridor, wheezes, decreased peripheral vascular resistance, and increased bowel sounds on examination.
Septic shock occurs when
gram-positive or gram-negative bacterial infection (or occasionally, fungi or viruses) overwhelms the body's defense mechanisms
This is a dreaded complication for individuals who suffer from
- severe trauma,
- immunodeficiency syndromes,
- or are very young or elderly.

These types of individuals are often unable to eradicate a localized infection such that it spreads into the bloodstream, causing bacteremia.
Etiology
The most common source for gram-negative organisms entering into the bloodstream is the
urinary tract, especially in individuals with indwelling urinary catheters.
Gram-positive bacteremia has become even more common than gram-negative infections because of
the increase in percutaneous (through skin) indwelling vascular catheters which are susceptible to contamination by gram-positive organisms on the skin.
In the intensive care unit, both gram-negative and gram-positive organisms can cause
pneumonia, especially in those individuals undergoing mechanical ventilation.
Gram-negative organisms that enter the bloodstream release what?
Endotoxin (lipopolysaccharide) from their cell walls
Gram-positive organisms release what?
Exotoxin and cell wall components such as peptidoglycan and teichoic acid.
These substances activate macrophages by binding to
specialized receptors in the surface of macrophages called toll-like receptors (TLR2 and TLR4)

The activated macrophages release inflammatory cytokines.
Some of the most important macrophage-derived inflammatory cytokines include
- tumor necrosis factor-alpha (TNF-alpha), - interleukins, and
- nitric oxide.

The complement and coagulation systems are also activated.

This results in what is called the systemic inflammatory response syndrome, or SIRS
SIRS, is manifested clinically by
fever, tachypnea, tachycardia, and leukocytosis.
A constellation of cell and tissue complications results, including
- decreased peripheral resistance, - decreased cardiac output,
- and increased capillary permeability,

all of which cause hypotension and decreased tissue perfusion.

Lactic acidosis, widespread coagulation, and activation of other inflammatory cells also occur.
Finally, organ dysfunction involving many of the vital organs can become
overwhelming and cause death. Some of the most common manifestations of multiple organ dysfunction syndrome or MODS are

- Acute respiratory distress syndrome (ARDS)
- Disseminated intravascular coagulation (DIC)
- Acute tubular necrosis (ATN)
- Liver and heart failure
- Central nervous system (CNS) dysfunction
Individuals with hypotension and septic shock initially present with:

Initial Clinical Manifestations
Evidence of a source of infection
—fever, tachypnea, tachycardia

Decreased peripheral vascular resistance
—warm, sweaty skin
As the SIRS & organ dysfunction progress, the individual may exhibit the clinical manifestations associated with multiple organ dysfunction:

Progressive Disease Clinical Manifestations
ARDS—increasing dyspnea, pulmonary crackles, and cyanosis

DIC—organ infarction and bleeding

ATN—decreased urine output

CNS dysfunction—confusion and coma
Laboratory evaluations frequently reveal:
Leukocytosis—elevated white blood cell count

Lactic acidosis—low pH, elevated lactate levels

Hypoxemia—abnormally low oxygen level

Uremia—elevated blood urea nitrogen and creatinine

Hepatic insufficiency—elevated liver enzymes

Bleeding from stress ulcers of the upper gastrointestinal tract is also common.
Management requires the prompt administration of
antibiotics, oxygen, pressors, and careful fluid management.

An anti-inflammatory and anticoagulant drug called activated protein C has been one of the first medications to improve outcomes in severe sepsis.
Cardiogenic Shock Clinical Manifestations
- dyspnea
- inspiratory crackles
- cyanosis
- cold/clammy extremities
- poor cap refill
- oliguria
Hypovolemic Clinical Manifestations
- cold/clammy extremities
- poor cap refill
- oliguria
Neurogenic Clinical Manifestations
- decreased peripheral vasc resistance
- bradycardia
Anaphylactic Clinical Manifestations
- decreased peripheral vasc resistance
- wheezes
- stridor
- overactive bowel sounds
Septic Clinical Manifestations
- evidence of source of infection
- fever
- decreased peripheral vasc resistance
- evidence of ARDS, DIC
Cardiogenic Shock Treatment
- treatment of underlying condition
- pressors
- careful fluid management
- ventricular assist devices
Hypovolemic Shock Treatment
- reversal of underlying condition of volume loss
- IV fluids (blood if indicated)
Neurogenic Shock Treatment
- careful patient positioning
- pressors
- careful fluid management
- - reversal of underlying condition
Anaphylactic Shock Treatment
- epinephrine
- corticosteroids
- fluids
- bronchodilators
- ventilation
Septic Shock Treatment
- antibiotics
- fluids
- pressors
- ventilation
- activated protein C
Multiple organ dysfunction syndrome (MODS) is defined as the
progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury.
Which shock is the most common cause of SIRS and MODS
Septic shock

but these complications can occur in other insults such as trauma, burns, and other causes of severe shock with underperfusion of vital tissues.
Multiple organ dysfunction syndrome (MODS): some of the most commonly affected organs include
the lung (acute respiratory distress syndrome [ARDS]),

- the hematologic system (disseminated intravascular coagulation [DIC]),

the kidney (acute tubular necrosis [ATN]),

the liver (hepatic failure),

and the gut (ischemic bowel, translocation of bacteria into the bloodstream).
Multiple organ dysfunction syndrome (MODS) Management includes
- reversal of the primary insult if possible -
- and support for organ failure including -

mechanical ventilation,
activated protein C,
dialysis,
fluid and electrolyte management,
enteral or parenteral nutrition,
and antibiotics.