CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology.

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CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology

Transcript of CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology.

Page 1: CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology.

CHAPTER 23

DISORDERS OF VENTILATION AND GAS EXCHANGE

Essentials of Pathophsiology

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PRE LECTURE QUIZ TRUE/FALSE

Pleural, musculoskeletal, and myocardial pain are similar in description and almost impossible to differentiate.

Extrinsic or atopic asthma is typically initiated by a type I hypersensitivity reaction induced by exposure to an extrinsic antigen or allergen, such as dust mite allergens, cockroach allergens, and animal dander.

Persons with emphysema are often labeled as “blue bloaters” because of the chronic hypoxemia and eventual right-sided heart failure with peripheral edema.

Cystic fibrosis is manifested by pancreatic exocrine deficiency and a noted decrease in levels of sodium chloride in the sweat.

Hypercapnia refers to an abnormal increase in oxygen levels.

F

T

F

F

F

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PRE LECTURE QUIZ

A pleural __________ refers to an abnormal collection of fluid in the pleural cavity.

__________ is a leading cause of chronic illness in children and is responsible for a significant number of lost school days; it is also the most frequent admitting diagnosis in children’s hospitals.

A __________ pneumothorax, a life-threatening condition, occurs when the intrapleural pressure exceeds atmospheric pressure, permitting air to enter but not leave the pleural space.

A pulmonary __________ develops when a blood-borne substance lodges in a branch of the pulmonary artery and obstructs the flow.

Cor pulmonale refers to __________-sided heart failure resulting from primary lung disease and involves hypertrophy and eventual failure of that ventricle.

Asthma

Effusion

Embolism

Right

Tension

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CAUSES OF RESPIRATORY FAILURE

Hypoventilation hypercapnia, hypoxia Depression of the respiratory center Diseases of respiratory nerves or muscles Thoracic cage disorders

Ventilation–perfusion mismatching Impaired diffusion hypoxemia but not

hypercapnia Interstitial lung disease ARDS Pulmonary edema Pneumonia

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HYPOXEMIA

PO2 <60 mm Hg

Cyanosis

Impaired function of vital centers Agitated or combative behavior, euphoria,

impaired judgment, convulsions, delirium, stupor, coma

Retinal hemorrhage

Hypotension and bradycardia

Activation of compensatory mechanisms Sympathetic system activation

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HYPERCAPNIA

PCO2 >50 mm Hg

Respiratory acidosis Increased respiration Decreased nerve firing

º Carbon dioxide narcosis

º Disorientation, somnolence, coma

Decreased muscle contractionº Vasodilation

Headache; conjunctival hyperemia; warm, flushed skin

CO2 + H2O H2CO3 H+ + HCO3-

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QUESTION

Tell whether the following statement is true or false.

Both hypercapnia and hypoxemia will lead to respiratory failure if untreated.

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ANSWER

TrueRationale: In hypercapnia (PCO2 >50

mm Hg), tissues accumulate carbon dioxide; in hypoxemia (PO2 <60 mm Hg), less oxygen is delivered to the tissues. In both cases, gas exchange is impaired, and respiratory failure will result unless the conditions are corrected (with oxygen, mechanical ventilation, etc.).

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PLEURAL DISORDERS DECREASE VENTILATION Parietal pleura lines

the thoracic wall and superior aspect of the diaphragm

Visceral pleura covers the lung

Pleural cavity or space between the two layers contains a thin layer of serous fluid

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SCENARIO

Mr. K presents himself with a stab wound

Now he is having breathing problems, and his breath sounds are diminished on the side with the wound

His trachea seems to be slanting toward the other side of his chest, and his heart sounds are displaced away from the wound

He has an increased respiration rate and blood pressure, is pale and sweating with bluish nail beds, and has no bowel sounds

Question:

Explain the effects of the wound

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PNEUMOTHORAX

Air enters the pleural cavity Air takes up space, restricting lung

expansion Partial or complete collapse of the

affected lung Spontaneous: an air-filled blister on the lung

ruptures Traumatic: air enters through chest injuries

º Tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation

º Open: air enters pleural cavity through the wound on inhalation and leaves on exhalation

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OPEN PNEUMOTHORAX

Air Comes in

Air goes out

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TENSION PNEUMOTHORAX

Air comes in

Air is trapped

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QUESTION

Tell whether the following statement is true or false.

Open pneumothorax is more life-threatening than tension pneumothorax.

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ANSWER

FalseRationale: In open pneumothorax, inhaled air

compresses the affected side’s lung, but during exhalation, the lung reinflates somewhat. In tension pneumothorax, a sort of one-way valve exists: the air enters the affected side during inhalation, but is unable to leave when the patient exhales. Therefore, all of this air exerts increased pressure on the organs of the thoracic cage. Unless the pressure is relieved, tension pneumothorax is fatal.

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PLEURAL EFFUSION—FLUID IN THE PLEURAL CAVITY

Hydrothorax: serous fluid

Empyema(em-pī-ē-mə) : pus

Chylothorax: lymph Hemothorax: blood

an accumulation of fluid in one or both pleural cavities, often resulting from disease of the heart or kidneys

fluid in the pleural space secondary to leakage from the thoracic duct

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OBSTRUCTIVE AIRWAY DISORDERS

Bronchial asthma Chronic obstructive airway

diseases Chronic bronchitis Emphysema Bronchiectasis Cystic fibrosis

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PATHOGENESIS OF BRONCHIAL ASTHMA

Early Phase

AntigenIgECytokine ReleaseMuscle Spasm

Late Phase

Mast Cell ActivationVascular porosity Edema and WBC infiltrationEpithelial DamageMuscle Spasm with edema

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EXTRINSIC (ATOPIC) ASTHMA

Type I hypersensitivity Mast cells’

inflammatory mediators cause acute response within 10–20 minutes

Treat with inhalers Airway inflammation

causes late-phase response in 4–8 hours

Treat with antiflamatory

Allergen

Mast cells release inflammatory

mediators

WBCs enter region and release more

inflammatory mediators

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INTRINSIC (NONATOPIC) ASTHMA

Respiratory infections Epithelial damage, IgE production

Exercise, hyperventilation, cold air Loss of heat and water may cause

bronchospasm Inhaled irritants

Inflammation, vagal reflex Aspirin and other NSAIDs

Abnormal arachidonic acid metabolism

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AIRWAY OBSTRUCTION IN ASTHMA

inflammatory mediators

airway inflammation

bronchospasm

edema

impaired mucociliary

function

epithelial injury

increased airway

responsiveness

airflow limitation

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QUESTION

Which of the following occurs in asthma?a. Airway inflammationb. Bronchospasm c. Decreased ability to clear mucusd. All of the above

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ANSWER

d. All of the aboveRationale: Inflammatory mediators lead

to airway inflammation, edema of the mucous lining of the airways, bronchospasm, and impaired ability to clear secretions. All of these things cause the airways to narrow during an asthma attack.

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CHRONIC OBSTRUCTIVE PULMONARY DISORDERS

Emphysema Enlargement of air spaces and

destruction of lung tissue Chronic obstructive bronchitis

Obstruction of small airways Bronchiectasis

Infection and inflammation destroy smooth muscle in airways, causing permanent dilation

the bronchi are distended, characterized by sudden violent coughing and copious expectoration of sputum, and which often become infected

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MECHANISMS OF COPD

Inflammation and fibrosis of bronchial wall Hypertrophied mucus glands excess mucus

Obstructed airflow Loss of alveolar tissue

Decreased surface area for gas exchange Loss of elastic lung fibers

Airway collapse, obstructed exhalation, air trapping

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Mechanism of COPD

A) Inflammation, Fibrosis

B) Hypersecretion of mucus

C) Destruction of elastic fibers that hold the airways open

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EMPHYSEMA

Neutrophils in alveoli secrete trypsin Increased neutrophil numbers due to

inhaled irritants can damage alveoli Alpha1-antitrypsin inactivates the trypsin

before it can damage the alveoli A genetic defect in alpha1-antitrypsin

synthesis leads to alveolar damage

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TYPES OF EMPHYSEMA

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Emphysemia Chest Wall Shape

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CHRONIC BRONCHITIS

Chronic irritation of airways Increased number of mucus

cells Mucus hypersecretion

Productive cough

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PINK PUFFERS VS. BLUE BLOATERS

Pink puffers (usually emphysema) Increase respiration to maintain oxygen

levels Dyspnea; increased ventilatory effort Use accessory muscles; pursed-lip breathing

Blue bloaters (usually bronchitis) Cannot increase respiration enough to

maintain oxygen levels Cyanosis and polycythemia Cor pulmonale

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QUESTION

Which chronic obstructive pulmonary disease primarily affects the alveoli?

a. Asthmab. Emphysemac. Chronic bronchitisd. Bronchiectasis (dilitation)

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ANSWER

b. EmphysemaRationale: In emphysema, alveolar

walls are destroyed. The other chronic pulmonary diseases listed primarily affect the airways.

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COPD AND BLOOD PH

Discussion: In what range will a COPD client’s

blood pH fall? Why?

Normal when stabilized & down to 7.3 unstabilized

CO2 +H2O H2CO3 H+ + HCO3-

Respiratory acidosis(lung induced): Low pH, High CO2, Low HCO3-

Metabolic (tissue induced): Low pH, High CO2, Normal HCO3-

Venous blood gas

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CONSEQUENCES OF COPD Which step in this

flow chart will cause the central chemoreceptors to increase respiration?

Which will cause the peripheral chemoreceptors to increase respiration?

COPD

decreased ability to

exhale

stale air in lungs

low O2 levels

high CO2

levels

hypercapnia

hypoxia

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SCENARIO

A client with chronic bronchitis has a barrel chest and cyanosis. His pulse oximeter reads 86% oxygenation. His PO2 is 54 mm Hg. His PCO2 is 56 mm Hg.

He is put on low-flow oxygen but complains of shortness of breath. Somebody turns the O2 flow up. He is found in a coma with a PCO2 of 59 mm Hg and a blood pH of 7.2.

Question: What was the cause of the coma? Why?

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CYSTIC FIBROSIS

Recessive disorder in chloride transport proteins High concentrations of NaCl in the

sweat Less Na+ and water in respiratory

mucus and in pancreatic secretionsº Mucus is thicker

Obstructs airways Obstructs pancreatic and biliary

ducts

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PATHOGENESIS OF CYSTIC FIBROSIS

Cystic Fibrosis Transmembrane Regulator Gene Failure

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CYSTIC FIBROSIS MANIFESTATIONS

Discussion: A client with cystic fibrosis is having

respiratory problems and: Digestive problems Flatulence Steatorrhea Weight loss

Question: He does not understand why a respiratory

disease would cause these problems. How would this be explained to the client?

Steatorrhea is the presence of excess fat in feces. Stools may also float due to excess lipid, have an oily appearance and be especially foul smelling.

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PULMONARY BLOOD FLOW

In a COPD client, exhalation is inefficient and O2 levels in the lungs decrease

If blood goes through the lungs filled with stale air, it will not pick up much oxygen; it might even pick up CO2

Discussion: What will the pulmonary arterioles do? Which side of the heart will be affected? Why?

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DISORDERS OF PULMONARY BLOOD FLOW

Pulmonary embolism Pulmonary hypertension

Primaryº Blood vessel walls thicken and

constrict Secondary

º Elevation of pulmonary venous pressure

º Increased pulmonary blood flowº Pulmonary vascular obstructionº Hypoxemia

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PULMONARY EMBOLISM

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Results of Pulmonary Hypertension

Occluded pulmonary artery

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COR PULMONALE

Right-sided heart failure secondary to respiratory disease Decreased lung ventilation Pulmonary vasoconstriction Increased workload on right heart Decreased oxygenation Kidney releases erythropoietin more

RBCs made Polycythemia makes blood more viscous Increased workload on heart

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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Exudate enters alveoli Blocks gas exchange Makes inhalation more

difficult Neutrophils enter alveoli

Release inflammatory mediators

Release proteolytic enzymes

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MECHANISMS OF LUNG CHANGES IN ARDS

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QUESTION

Tell whether the following statement is true or false.

Patients suffering from ARDS will be not necessarily be hypoxemic.

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ANSWER

FalseRationale: In ARDS the alveoli are filled

with exudate, decreasing the available surface area for gas exchange. If gas exchange decreases, poorly oxygenated or unoxygenated blood is sent to the tissues (hypoxemia).