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Title: Division 1 Introduction to Advanced Prehospital Care


1
Division 1Introduction to AdvancedPrehospital
Care
2
Chapter 4General Principles of
PathophysiologyPart I How Normal Body Processes
Are Altered by Disease and Injury
3
Topics
  • Disease Risk
  • Hypoperfusion
  • Shock
  • Multiple Organ Dysfunction Syndrome

4
Pathophysiology
  • The study of how diseases alter the normal
    physiological processes of the human body
  • From the root patho meaning disease

5
How Cells Respond to Change and Injury
6
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,
    dilation of the left ventricle after an MI.

7
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

8
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

9
Cellular Injury
  • Hypoxic
  • Chemical
  • Infectious
  • Immunologic/Inflammatory
  • Physical agents
  • Nutritional balances
  • Genetic factors

10
Manifestation of Cellular Injury
  • When cells are injured metabolism is changed,
    causing substances to infiltrate or accumulate to
    an abnormal degree in cells.

11
Cellular Swelling
  • Results from a permeable or damaged cellular
    membrane
  • Caused by an inability to maintain stable intra-
    and extracellular fluid and electrolyte levels

12
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.

13
Signs and Symptoms of Cellular Change
  • Fatigue and malaise
  • Altered appetite
  • Fever
  • Increased heart rate associated with fever
  • Pain

14
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.

15
Cell Death (2 of 3)
  • Necrosis
  • A pathological process
  • Cells swell and rupture
  • Coagulative
  • Liquefactive
  • Caseous
  • Fatty

16
Cell Death (3 of 3)
  • Gangrenous necrosis
  • Cell death over a wide area
  • Dry
  • Wet
  • Gas

17
Fluids and Fluid Imbalances
18
Water is the most abundant substance in the human
body.
19
Where the Water Is Found
  • Intracellular fluidfluid inside the cells
  • Extracellular fluidall the fluid outside the
    body cells
  • Intravascular fluidfluid within the circulatory
    system
  • Interstitial fluidfluid outside of the cell
    membranes but not within the circulatory system

20
Edema
  • Accumulation of water in the interstitial space
    due to disruption in the forces and mechanisms
    that normally keep net filtration at zero

21
Mechanisms That Cause Edema
  • A decrease in plasma oncotic force
  • An increase in hydrostatic pressure
  • Increased capillary permeability
  • Lymphatic channel obstruction

22
Edema (1 of 2)
  • Can be local or within a certain organ system
  • Sprained ankle vs. pulmonary edema

23
Edema (2 of 2)
  • Water in interstitial spaces is not available for
    metabolic processes.
  • Edema, therefore, can cause a relative condition
    of dehydration.

24
Intravenous Therapy
25
Blood Components
26
The percentage of the blood occupied by the red
blood cells is termed the hematocrit.
27
Fluid Replacement
28
Transfusion Reactions
  • Transfusion reactions occur when there is a
    discrepancy between the blood type of the patient
    and the type of the blood being transfused.

29
Signs and Symptoms of Transfusion Reactions
  • Fever
  • Chills
  • Hives
  • Hypotension
  • Palpitations
  • Tachycardia
  • Flushing of the skin
  • Headache
  • Loss ofconsciousness
  • Nausea
  • Vomiting
  • Shortness of breath

30
Treatment of Transfusion Reactions (1 of 2)
  • IMMEDIATELY stop the transfusion.
  • Save the substance being transfused.
  • Rapid IV infusion.

31
Treatment of Transfusion Reactions (2 of 2)
  • Assess the patients mental status.
  • Administer oxygen.
  • Contact medical direction.
  • Be prepared to administer mannitol,
    diphenhydramine, or furosemide.

32
Intravenous Fluids
33
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
  • PolyHeme
  • Hemopure

34
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)

35
Crystalloids
  • Crystalloid solutions are the primary compounds
    used in prehospital care.
  • Isotonic solutions
  • Hypertonic solutions
  • Hypotonic solutions

36
The effects of hypertonic, isotonic, and
hypotonic solutions on red blood cells
37
Most Commonly Used Solutions in Prehospital Care
Solution Tonicity
Lactated Ringers Isotonic
Normal Saline Isotonic
D5W Hypotonic
38
Acid-Base Derangements
39
Respiratory Acidosis
  • Caused by abnormal retention of CO2 from
    impaired ventilation due to problems occurring in
    the lungs or respiratory center of the brain.

40
Respiratory Alkalosis
Caused by increased respiration and excessive
elimination of CO2. The CO2 level is decreased
and the pH is increased.
41
Metabolic Acidosis
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.
42
Compensation for metabolic acidosis begins with
an increase in respirations.
43
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.

44
Genetics and Other Causes of Disease
45
Many Factors Combine to Cause Disease (1 of 3)
  • Genetics
  • Environment
  • Lifestyle
  • Age
  • Gender

46
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.

47
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.

48
  • Most disease processes are multifactorial in
    origin.

49
Disease Effects on Individuals
  • Host
  • Agent
  • Environment

50
Disease Effects on Populations
  • Incidence
  • Prevalence
  • Mortality

51
Family History and Associated Risk Factors
52
Immunologic Disorders
  • A number of immunologic disorders are more
    prevalent among those with a family history of
    the disorder.

53
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

54
Endocrine Disorders
  • The most common endocrine disorder is diabetes
    mellitus.
  • Leading cause of
  • Blindness
  • Heart disease
  • Kidney failure
  • Premature death
  • Both Type I and Type II diabetes can be family
    related.

55
Hematological Disorders
  • There are many causes of hereditary hematological
    disorders such as gene alteration and
    histocompatibility (tissue interaction)
    dysfunctions.
  • Hemophilia
  • Hemochromatosis

56
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

57
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

58
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.

59
Gastrointestinal Disorders
  • Lactose intolerance
  • Crohns disease
  • Peptic ulcers
  • Cholecystitis
  • Obesity

60
Neuromuscular Disorders
  • Diseases of the nervous and muscular systems
    include
  • Huntingtons disease
  • Multiple sclerosis
  • Alzheimers disease

61
Psychiatric Disorders
  • Genetic and biological causes of these disorders
    are being studied and increasingly understood.
  • Schizophrenia
  • Manic-depressive illness (bipolar disorder)

62
Hypoperfusion
63
  • Hypoperfusion (shock) is inadequate perfusion of
    body tissues.

64
Progression of Shock
65
The Pathophysiology of Hypoperfusion
66
Causes of Hypoperfusion (1 of 3)
  • Inadequate pump
  • Inadequate preload
  • Inadequate cardiac contractile strength
  • Excessive afterload

67
Causes of Hypoperfusion (2 of 3)
  • Inadequate fluid
  • Hypovolemia

68
Causes of Hypoperfusion (3 of 3)
  • Inadequate container
  • Dilated container without change in fluid volume
    (inadequate systemic vascular resistance)
  • Leak in the container

69
Shock at the Cellular Level
  • Shock causes vary however, the ultimate outcome
    is impairment of cellular metabolism.

70
Impaired Use of Oxygen
  • When cells dont receive enough oxygen or cannot
    use it effectively, they change from aerobic to
    anaerobic metabolism.

71
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.

72
Glucose Breakdown (2 of 2)
  • 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 produces a much higher yield of
    energy.

73
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.

74
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).

75
Shock Variations (1 of 3)
  • Compensated shock is the early stage of shock
    during which the bodys compensatory mechanisms
    are able to maintain normal perfusion.

76
Shock Variations (2 of 3)
  • Decompensated shock is an advanced stage of shock
    that occurs when the bodys compensatory
    mechanisms no longer maintain normal perfusion.

77
Shock Variations (3 of 3)
  • Irreversible shock is shock that has progressed
    so far that the body and medical intervention
    cannot correct it.

78
Types of Shock
  • Cardiogenic
  • Hypovolemic
  • Neurogenic
  • Anaphylactic
  • Septic

79
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.

80
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.

81
Cardiogenic Shock Treatment (1 of 2)
  • Assure an open airway.
  • Administer oxygen.
  • Assist ventilations as necessary.
  • Keep the patient warm.

82
Cardiogenic Shock Treatment (2 of 2)
  • Elevate the patients head and shoulders.
  • Establish IV access with minimal fluid
    administration.
  • Monitor the heart rate.
  • Dopamine or dobutamine may be administered.

83
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

84
Hypovolemic Shock Evaluation (1 of 2)
  • Altered level of consciousness.
  • Pale, cool, clammy skin.
  • Blood pressure may be normal, then fall.

85
Hypovolemic Shock Evaluation (2 of 2)
  • Pulse may be normal then become rapid, finally
    slowing and disappearing.
  • Urination decreases.
  • Cardiac dysrhythmias may occur.

86
Hypovolemic Shock Treatment
  • Airway control.
  • Control severe bleeding.
  • Keep the patient warm.
  • Administer a bolus of crystalloid solution for
    fluid replacement.
  • Non-trauma 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.

87
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.

88
Neurogenic Shock Evaluation
  • Warm, dry, red skin
  • Low blood pressure
  • Slow pulse

89
Neurogenic Shock Treatment
  • Airway control.
  • Maintain body temperature.
  • Immobilization of patient.
  • Consider other possible causes of shock.
  • IV access and medications that increase
    peripheral vascular resistance.

90
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, hornets

91
Anaphylactic Shock Evaluation
  • Cardiovascular system
  • Vasodilation, increased heart rate, decreased
    blood pressure
  • Gastrointestinal system
  • Nausea, vomiting, abdominal cramping, diarrhea
  • Nervous system
  • Altered mental status, dizziness, headache,
    seizures, tearing

92
Anaphylactic Shock Treatment
  • Airway protection may includeendotracheal
    intubation.
  • Establish an IV of crystalloidsolution.
  • Pharmacological intervention
  • Epinephrine, antihistamines, corticosteroids,
    vasopressors, inhaled beta agonists

93
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.

94
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

95
Septic Shock Treatment
  • Airway control.
  • IV of crystalloid solution.
  • Dopamine to support blood pressure.
  • Monitor heart rhythm.

96
Multiple Organ Dysfunction Syndrome
  • MODS is the progressive impairment of two or more
    organ systems from an uncontrolled inflammatory
    response to a severe illness or injury.

97
MODS Stages
98
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.

99
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.

100
MODS 24 Hours after Resuscitation
  • Low grade fever
  • Tachycardia
  • Dyspnea
  • Altered mental status
  • General hypermetabolic, hyperdynamic state

101
MODS within 24 to 72 Hours
  • Pulmonary failure begins.

102
MODS within 7 to 10 Days
  • Hepatic failure begins.
  • Intestinal failure begins.
  • Renal failure begins.

103
MODS within 14 to 21 Days
  • Renal and hepatic failure intensify.
  • Gastrointestinal collapse.
  • Immune system collapse.

104
MODS after 21 Days
  • Hematological failure begins.
  • Myocardial failure begins.
  • Altered mental status resulting from
    encephalopathy.
  • Death.

105
Summary
  • Disease Risk
  • Hypoperfusion
  • Shock
  • Multiple Organ Dysfunction Syndrome
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