CHAPTER 4 POWERPOINT/PARAMEDIC STUDY

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Bledsoe/Porter/Cherry, Essentials of Paramedic Care, Second Edition Update © 2011 by Pearson Education, Inc. Upper Saddle River, New Jersey Division 1 Introduction to Advanced Prehospital Care

Transcript of CHAPTER 4 POWERPOINT/PARAMEDIC STUDY

Bledsoe/Porter/Cherry, Essentials of Paramedic Care, Second Edition Update© 2011 by Pearson Education, Inc. Upper Saddle River, New Jersey

Division 1Introduction to Advanced

Prehospital Care

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Chapter 4General Principles of

PathophysiologyPart I

How Normal Body Processes Are Altered by Disease and Injury

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Topics

Disease Risk

Hypoperfusion

Shock

Multiple Organ Dysfunction Syndrome

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Pathophysiology

The study of how diseases alter the normal physiological processes of the human body

From the root “patho” meaning disease

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How Cells Respond to Change and Injury

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Cellular Adaptation

Cells, tissues, organs, and organ systems can adapt to both normal and injurious conditions.Adaptation to external stressors results in alteration of structure and function.Examples: growth of the uterus during pregnancy and, dilation of the left ventricle after an MI.

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Types of Cellular Adaptations(1 of 2)

Atrophy– Decreased size resulting from a decreased

workload

Hypertrophy– An increase in cell size resulting from an

increased workload

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Types of Cellular Adaptations(2 of 2)

Hyperplasia– An increase in the number of cells

resulting from an increased workload

Metaplasia– Replacement of one type of cell by

another type of cell that is not normal for that tissue

Dysplasia– A change in cell size, shape, or

appearance caused by an external stressor

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Cellular Injury

Hypoxic

Chemical

Infectious

Immunologic/inflammatory

Physical agents

Nutritional balances

Genetic factors

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Manifestation of Cellular Injury

When cells are injured, metabolism is changed, causing substances to infiltrate or accumulate to an abnormal degree in cells.

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Cellular Swelling

Results from a permeable or damaged cellular membrane

Caused by an inability to maintain stable intra- and extracellular fluid and electrolyte levels

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Fatty Change

Lipids invade the area of injury.

Occurs most commonly in vascular organs, most frequently the liver.

Causes a disruption of the cellular membrane and metabolism and interferes with the vital functions of the organ.

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Signs and Symptoms of Cellular Change

Fatigue and malaise

Altered appetite

Fever

Increased heart rate associated with fever

Pain

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Cell Death (1 of 3)

Apoptosis– Injured cell releases enzymes that engulf

and destroy the cell.– Cells shrink.– Eliminating damaged and dead cells

allows tissues to repair and possibly regenerate.

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Cell Death (2 of 3)

Necrosis– A pathological process

– Cells swell and rupture– Coagulative– Liquefactive– Caseous– Fatty

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Cell Death (3 of 3)

Gangrenous necrosis– Cell death over a wide area

– Dry– Wet– Gas

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Fluids and Fluid Imbalances

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Water is the most abundant substance in the human body.

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Where the Water Is Found

Intracellular fluid—fluid inside the cells

Extracellular fluid—all the fluid outside the body cells– Intravascular fluid—fluid within the

circulatory system– Interstitial fluid—fluid outside of the cell

membranes but not within the circulatory system

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Edema

Accumulation of water in the interstitial space due to disruption in the forces and mechanisms that normally keep net filtration at zero

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Mechanisms That Cause Edema

A decrease in plasma oncotic force

An increase in hydrostatic pressure

Increased capillary permeability

Lymphatic channel obstruction

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Edema (1 of 2)

Can be local or within a certain organ system– Sprained ankle vs. pulmonary edema

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Edema (2 of 2)

Water in interstitial spaces is not available for metabolic processes.

Edema, therefore, can cause a relative condition of dehydration.

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Intravenous Therapy

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Blood Components

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The percentage of the blood occupied by the red blood cells is termed the hematocrit.

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Fluid Replacement

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Transfusion reactions occur when there is a discrepancy between the blood type of the patient and the type of the blood being transfused.

Transfusion Reactions

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Signs and Symptoms of Transfusion Reactions

Fever

Chills

Hives

Hypotension

Palpitations

Tachycardia

Flushing of the skin

Headache

Loss ofconsciousness

Nausea

Vomiting

Shortness of breath

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Treatment of Transfusion Reactions (1 of 2)

IMMEDIATELY stop the transfusion.

Save the substance being transfused.

Rapid IV infusion.

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Treatment of Transfusion Reactions (2 of 2)

Assess the patient’s mental status.

Administer oxygen.

Contact medical direction.

Be prepared to administer mannitol, diphenhydramine, or furosemide.

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Intravenous Fluids

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Hemoglobin-Based Oxygen-Carrying Solutions (HBOCs)

Commonly referred to as “blood substitutes”– Compatible with all blood types– Do not require blood typing, testing, or

cross-matching

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Colloids

Colloids remain in intravascular spaces for an extended period of time and have oncotic force.– Plasma protein fraction (Plasmanate)– Salt-poor albumin– Dextran– Hetastarch (Hespan)

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Crystalloids

Crystalloid solutions are the primary compounds used in prehospital care.– Isotonic solutions– Hypertonic solutions– Hypotonic solutions

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The effects of hypertonic, isotonic, and hypotonic solutions

on red blood cells

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Most Commonly Used Solutions in Prehospital Care

Solution Tonicity

Lactated Ringer Isotonic

Normal saline Isotonic

D5W Hypotonic

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Acid-Base Derangements

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Caused by abnormal retention of CO2 from impaired ventilation due to problems occurring in the lungs or respiratory center of the brain.

Respiratory Acidosis

Respiration = CO2 + H2O H2CO3 H+ + HCO3–

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Caused by increased respiration and excessive elimination of CO2. The CO2 level is decreased and the pH is increased.

Respiratory Alkalosis

Respiration = CO2 + H2O H2CO3 H+ + HCO3–

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Results from the production of metabolic acids such as lactic acid. These acids consume bicarbonate ions.

Can be the result of dehydration, diabetes, or medication usage.

Metabolic Acidosis

H+ + HCO3– H2CO3 H2O + CO2

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Compensation for metabolic acidosis begins with an increase in respirations.

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Metabolic Alkalosis

The pH is increased and the CO2 level is normal. It is usually caused by administration of diuretics, loss of chloride ions associated with prolonged vomiting, and overzealous administration of sodium bicarbonate.

H+ + HCO3– H2CO3 H2O + CO2

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Genetics and Other

Causes of Disease

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Many Factors Combine to Cause Disease (1 of 3)

Genetics

Environment

Lifestyle

Age

Gender

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Many Factors Combine to Cause Disease (2 of 3)

Inherited traits are determined by molecules of deoxyribonucleic acid (DNA).

Each somatic cell contains 46 chromosomes.

Sex cells contain 23 chromosomes.

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Many Factors Combine to Cause Disease (3 of 3)

An offspring receives 23 chromosomes from the mother and 23 chromosomes from the father.

One or more chromosomes may be abnormal and may cause a congenital disease or a propensity toward acquiring a disease later in life.

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Most disease processes are multifactorial in origin.

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Disease Effects on Individuals

Host

Agent

Environment

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Disease Effects on Populations

Incidence

Prevalence

Mortality

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Family History and Associated Risk Factors

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Immunologic Disorders

A number of immunologic disorders are more prevalent among those with a family history of the disorder.

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Cancer

Some types of cancer tend to cluster in families and seem to have a combination of genetic and environmental causes.– Breast cancer– Colorectal cancer

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Endocrine Disorders

The most common endocrine disorder is diabetes mellitus.

If it is the leading cause of:– Blindness– Heart disease– Kidney failure– Premature death

Both type I and type II diabetes can be family related.

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Hematological Disorders

There are many causes of hereditary hematological disorders such as gene alteration and histocompatibility (tissue interaction) dysfunctions.– Hemophilia– Hemochromatosis

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Cardiovascular Disorders

The cardiovascular system can be greatly affected by genetic disorders.– Elongation of the QT interval– Mitral valve prolapse– Coronary artery disease– Hypertension– Cardiomyopathy

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Renal Disorders

Caused by a variety of factors, primarily hypertension.

EMS is increasingly being called upon to deal with complications of dialysis including:– Problems with vascular access devices– Localized infection and sepsis– Electrolyte imbalances

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Rheumatic Disorders

Gout is a disorder both genetic and environmental, characterized by the deposit of crystals in the joints, most commonly the great toe.

The crystals form as a result of abnormally high levels of uric acid in the blood.

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Gastrointestinal Disorders

Lactose intolerance

Crohn disease

Peptic ulcers

Cholecystitis

Obesity

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Neuromuscular Disorders

Diseases of the nervous and muscular systems include:– Huntington disease– Multiple sclerosis– Alzheimer disease

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Psychiatric Disorders

Genetic and biological causes of these disorders are being studied and increasingly understood.– Schizophrenia– Manic-depressive illness (bipolar

disorder)

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Hypoperfusion

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Hypoperfusion (shock) is inadequate perfusion of body tissues.

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Progression of Shock

Cellular Death

Tissue Death

Organ Death

Organ System Death

Organism Death

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The Pathophysiology of Hypoperfusion

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Causes of Hypoperfusion (1 of 3)

Inadequate pump– Inadequate preload

– Inadequate cardiac contractile strength– Excessive afterload

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Causes of Hypoperfusion (2 of 3)

Inadequate fluid– Hypovolemia

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Causes of Hypoperfusion (3 of 3)

Inadequate container– Dilated container without change in fluid

volume (inadequate systemic vascular resistance)

– Leak in the container

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Shock at the Cellular Level

Shock causes vary; however, the ultimate outcome is impairment of cellular metabolism.

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Impaired Use of Oxygen

When cells dont receive enough oxygen or cannot use it effectively, they change from aerobic to anaerobic metabolism.

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Glucose Breakdown (1 of 2)

Stage one, glycolysis, is anaerobic (does not require oxygen). It yields pyruvic acid, with toxic by-products such as lactic acid, and very little energy.

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Stage two is aerobic (requires oxygen). In a process called the Krebs or citric acid cycle, pyruvic acid is degraded into carbon dioxide and water, which produce a much higher yield of energy.

Glucose Breakdown (2 of 2)

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Compensation and Decompensation

Usually the body is able to compensate for any changes. However, when the various compensatory mechanisms fail, shock develops and may progress.

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Compensation Mechanisms

The catecholamines epinephrine and norepinephrine may be secreted.

The renin-angiotensin system aids in maintaining blood pressure.

Another endocrine response by the pituitary gland results in the secretion of anti-diuretic hormone (ADH).

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Shock Variations (1 of 3)

Compensated shock is the early stage of shock during which the body’s compensatory mechanisms are able to maintain normal perfusion.

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Shock Variations (2 of 3)

Decompensated shock is an advanced stage of shock that occurs when the body’s compensatory mechanisms no longer maintain normal perfusion.

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Shock Variations (3 of 3)

Irreversible shock is shock that has progressed so far that the body and medical intervention cannot correct it.

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Types of Shock

Cardiogenic

Hypovolemic

Neurogenic

Anaphylactic

Septic

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Cardiogenic Shock

The heart loses its ability to supply all body parts with blood.

Usually the result of left ventricular failure secondary to acute myocardial infarction or CHF.

Many patients will have normal blood pressures.

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Cardiogenic Shock Evaluation

The major difference between cardiogenic shock and other types of shock is the presence of pulmonary edema causing:– Difficulty breathing.– As fluid levels rise, wheezes or crackles

(rales) may be heard.– There may be a productive cough with

white or pink-tinged foamy sputum.– Cyanosis, altered mentation, and oliguria.

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Cardiogenic Shock Treatment (1 of 2)

Assure an open airway.

Administer oxygen.

Assist ventilations as necessary.

Keep the patient warm.

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Cardiogenic Shock Treatment (2 of 2)

Elevate the patient’s head and shoulders.

Establish IV access with minimal fluid administration.

Monitor the heart rate.

Dopamine or dobutamine may be administered.

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Hypovolemic Shock

Shock due to loss of intravascular fluid– Internal or external hemorrhage– Trauma– Long bones or open fractures– Dehydration– Plasma loss from burns– Excessive sweating– Diabetic ketoacidosis with resultant

osmotic diuresis

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Hypovolemic Shock Evaluation (1 of 2)

Altered level of consciousness.

Pale, cool, and clammy skin.

Blood pressure may be normal, then fall.

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Hypovolemic Shock Evaluation (2 of 2)

Pulse may be normal then become rapid, finally slowing and disappearing.

Urination decreases.

Cardiac dysrhythmias may occur.

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Hypovolemic Shock Treatment

Maintain airway control.Control severe bleeding.Keep the patient warm.Administer a bolus of crystalloid solution for fluid replacement.– Nontrauma or no blood loss

Bolus crystalloid or colloid solutions

– Trauma or blood loss“Permissive hypotension” – SBP of 70-85 mmHg

PASG if part of local protocol.

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Neurogenic Shock

Results from injury to brain or spinal cord causing an interruption of nerve impulses to the arteries.

The arteries dilate, causing relative hypovolemia.

Sympathetic impulses to the adrenal glands are lost, preventing the release of catecholamines with their compensatory effects.

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Neurogenic Shock Evaluation

Warm, dry, and red skin

Low blood pressure

Slow pulse

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Neurogenic Shock Treatment

Maintain airway control.

Maintain body temperature.

Immobilization of the patient.

Consider other possible causes of shock.

IV access and medications that increase peripheral vascular resistance.

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Anaphylactic Shock

A severe immune response to a foreign substance.

Signs and symptoms most often occur within a minute, but can take up to an hour.

The most rapid reactions are in response to injected substances– Penicillin injections– Bees, wasps, and hornets

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Anaphylactic Shock Evaluation

Cardiovascular system– Vasodilation, increased heart rate, and

decreased blood pressure

Gastrointestinal system– Nausea, vomiting, abdominal cramping,

and diarrhea

Nervous system– Altered mental status, dizziness,

headache, seizures, and tearing

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Anaphylactic Shock Treatment

Airway protection; may includeendotracheal intubation.

Establish an IV of crystalloidsolution.

Pharmacological intervention– Epinephrine, antihistamines,

corticosteroids, vasopressors, and inhaled beta-agonists

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Septic Shock

An infection that enters the bloodstream and is carried throughout the body.

The toxins released overcome the compensatory mechanisms.

Can cause the dysfunction of an organ system or result in multiple organ dysfunction syndrome.

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Septic Shock Evaluation

The signs and symptoms are progressive.– Increased to low blood pressure– High fever, no fever, or hypothermic– Skin flushed, pale, or cyanotic– Difficulty breathing and altered lung

sounds– Altered mental status

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Septic Shock Treatment

Maintain airway control.

Establish an IV of crystalloid solution.

Administer dopamine to support blood pressure.

Monitor heart rhythm.

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Multiple Organ Dysfunction Syndrome (MODS)

MODS is the progressive impairment of two or more organ systems from an uncontrolled inflammatory response to a severe illness or injury.

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MODS Stages

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Primary MODS

Organ damage results directly from a specific cause such as ischemia or inadequate tissue perfusion from shock, trauma, or major surgery.

Stress and inflammatory responses may be mild and undetectable.

During this response, neutrophils, macrophages, and mast cells are thought to be “primed” by cytokines.

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Secondary MODS

The next time there is an injury, ischemia, or infection, the primed cells are activated, producing an exaggerated inflammatory response.

The inflammatory response enters a self-perpetuating cycle causing damage and vasodilation.

An exaggerated neuroendocrine response is triggered causing further damage.

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MODS 24 Hours after Resuscitation

Low grade fever

Tachycardia

Dyspnea

Altered mental status

General hypermetabolic, hyperdynamic state

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MODS within 24 to 72 Hours

Pulmonary failure begins.

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MODS within 7 to 10 Days

Hepatic failure begins.

Intestinal failure begins.

Renal failure begins.

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MODS within 14 to 21 Days

Renal and hepatic failure intensify.

Gastrointestinal collapse.

Immune system collapse.

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MODS after 21 Days

Hematological failure begins.

Myocardial failure begins.

Altered mental status resulting from encephalopathy.

Death.

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Summary

Disease Risk

Hypoperfusion

Shock

Multiple Organ Dysfunction Syndrome