RTH 112Pathophysiology of the Cardiopulmonary Systems

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RTH 112-Pathophysiology of the Cardiopulmonary
Systems

• Joseph S. DiPietro, Ph.D., RRT
• Professor and Director, Respiratory Care Programs
• Co-Director, Health Technologys Education

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Pathophysiology

• The study of abnormal function and its
  relationship to disease
• In this course, our focus will be the
  cardiopulmonary systems
• Your text--Textbook of Pulmonary Disease, Baum

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Your responsibilities

• Pre-read your assignments before class
• We only have 9 and 1/4 weeks to cover 15 weeks of
  material
• Key to this--your preparation
• This is an open forum classroom--if your are not
  prepared, discussion with you will prove difficult

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Your responsibilities

• Much of the presentation will also tie in things
  youve already had, like physiology and physics
  and chemistry
• If you dont understand--
• ASK!!!!!!!!!!!!!!!

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Dont act like this person...
Worries, but does nothing to fix the problem,
until afterwards...
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U
Are ultimately responsible...for your grades
knowledge YOURSELF!!!
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The Obstructive Lung Diseases

• Bronchitis
• Emphysema
• Asthma

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Bronchitis

• Inflammation of the conducting zone airways
• Characterized by increased secretion production
• Considered chronic if...sputum production exists
  for three consecutive weeks for two consecutive
  months

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Features

• PaO2s lt 50 torr
• PaCO2s gt 50 torr
• pH normal (usually just shy of 7.40)
• increased secretions
• Old nickname blue bloater
• R heart failure, or right CHF (cor pulmonale)
• polycythemia
• increased A-P diameter due to air trapping
• Decreased breath sounds w/air trapping rhonchi

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Causes

• Inhalation of toxic gases
• SMOKING is the most common
• Inhalation of antigens
• Inhalation of viruses or bacteria

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Emphysema

• In Greek, this word means swollen with air
• There are two primary types of this disease
• Panlobar, which affects the acinus or alveolar
  groups-- usually a genetic predisposition due to
  Alpha 1, antitrypsin deficiency
• Centralobar, which affects respiratory
  bronchioles--smoking is the cause

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Features

• Increased A-P diameter
• Increased CO2s and decreased PO2s, late
• Old nickname pink puffer
• little or no secretions
• loss of gas surface area for diffusion
• skinny (the better term might be hyposthenic)
• Diminished breath sounds

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Causes

• SMOKING
• Genetics
• Bronchitis
• Asthma

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Pulmonary Function in Chronic Airways Obstruction

• Decreased expiratory flowrates such as the
  FEF200-1200 and FEF25-75 as well as FEV1
• Increased residual volume, functional residual
  capacity and total lung capacity
• Decreased capacity of diffusion DLCO

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Bronchitis v. Emphysema

• Easy to decompensate
• Usually relatively easy to treat
• Can cause emphysema
• Rarely are these patients ever having normal
  blood gases

• Usually more difficult to decompensate
• Difficult to treat
• Can be caused by bronchitis
• Early, blood gases are normal

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Gas Exchange is poor because

• Loss of alveolar structure base thereby causing
  decreased gas exchange surface area
• Mechanically, elastance is lost due to the
  constant stretching of distal airways
• Consequently, these patients are very compliant,
  because the natural tendency for the lung to
  collapse is inadvertently lost

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Asthma

• Known too, as the disease of reversible airways
  obstruction or reactive airways disease
• More deaths were associated with asthma in
  children in 1996 and 97 than in any time in
  documented history
• Commonly caused by the TYPE I Hypersensitivity
  Reaction or the Mast Cell Reaction

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Hypersensitivity Reactions

• TYPE I-- Mast cell degraulation resulting from
  antigen attachment and release of allergic
  mediators
• TYPE II--antigen-antibody complex seen in
  transfusion reactions
• TYPE III-- ARTHUS REACTION or localized
  antigen-antibody reactions such as hives
• TYPE IV-- delayed hypersensitivity such as
  pulmonary TB

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In Extrinsic Asthma (caused by an external source)

• The antigen attaches to the Mast Cell causing an
  antibody response (typically IgE)
• The mast cell degranulates and releases allergic
  mediators to remove the antigen

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The Released Mediators

• Histamine---causing bronchoconstriction
• Bradykinin--causing vasodilation
• Leukotrienes--causing bronchconstriction and
  vasodilation (Formerly known as SRS-A)
• ECF-A--Eosinophilic Chemotactic Factor of
  Anaphylaxis causing eosinophils to go to the
  sight of reaction
• PAF--Platelet Activating Factor causing
  production migration of platelets to sight of
  reaction
• Thromboxanes--causing bronchoconstriction and
  vasodilation

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The Mast Cell Reaction---

• Is a natural response in all people
• But in asthmatics, it is greatly accelerated
• Hence, hypersensitivity

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Asthma--the 2 types

• Extrinsic--caused by external sources such as
  pollen, bacteria, viruses, mold spores
• Instrinsic--caused by internal sources such as
  infection, chronic disease, stress phenomena

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Features

• Increased secretion production
• Bronchoconstriction
• WHEEZING
• prolonged expiration (increased ETime)
• air trapping
• initially, CO2s are decreased and so are PO2s
• Use of accessory muscles
• Breath sounds diminished crackles on insp.
• Increased A-P diameter barrelled chest

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Asthma-Pulmonary Function

• Decreased expiratory flow rates
• Increased residual volume, functional residual
  capacity, and total lung capacity
• Decreased diffusion
• Increased work of breathing

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Asthma-Rx

• Bronchodilators, parenteral and inhalants
• Adequate hydration
• In acute episodes, continuous bronchodilator
  aerosols
• steroids
• supplemental oxygen therapy
• if patient resistant to meds, this is known as
  STATIS ASTHMATICUS, and if CO2s are at 40 torr
  may need mechanical ventilation