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Pathophysiology > Lecture 35 - Respiratory > Flashcards

Lecture 35 - Respiratory Flashcards

1
Q

Define normal breathing

A

RR is 8-16 BPM
No accessory mm. use
Tidal Volume (Vt) = 400-800 BPM

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2
Q

Define dyspnea

A

Subjective discomfort of breathing often described as SOB or air hunger.

etiology: stimulation of central and peripheral chemoreceptors (pH of CSF; pH of blood; O2 receptors)

Disparity of tension generated by respiratory mm. and Vt

Clinical manifestations: flaring of nostrils, use of accessory mm., retraction of intercostal spaces and throat above sternum

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3
Q

Define Kussmaul respiration

A

Hypernea - slightly increased RR with large increase in Vt with no respiratory pauses

etiology: strenuous exercise, metabolic acidosis

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4
Q

Define Tachypnea

A

rapid RR with small Vt (also known as restricted breathing)

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5
Q

Define Cheyne Stokes Respiration

A

alternating shallow to deep then back to shallow respirations with apnea of 10-60 seconds between cresendos

Etiology: any condition that slows blood flow to brain (slows O2 to the brain); neurological impairment to the brain; occurs to everyone at high altitude

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6
Q

Define hypoventilation.

A

decreased alveolar ventilation –> hypercapnea (PaCO2 > 40 mm Hg)

Metabolic production of CO2 exceeds the ventilation’s CO2 removal by alveoli

*This is critical in diagnosis of pulmonary problems

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7
Q

Define hyperventilation

A

excessive alveolar ventilation –> hypocapnea (PaCO2

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8
Q

Be able to distinguish the breathing pattern of a person with Obstructive pulmonary disease
and a person with restrictive pulmonary disease

A

Obstructive pulmonary disease: this person will have decreased RR with and large Vt (usually because of prolonged expiratory phase more sos than prolonged inspiratory phase)

  • person can’t exhale all the air out of lungs

Restrictive pulmonary disease - tachypnea will occur or the RR will increase and Vt will be small

  • person can’t expand the lungs very well
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9
Q

Define/Delineate pulmonary changes that lead to Diffusion abnormalities of O2 and CO2
across the alveolar membranes

A

Normally O2 must cross through:

  1. Water Layer
  2. Type I alveolar cells
  3. Capillary Endothelium
  4. Basement membrane

Diffusion abnormalities:

  1. Pulmonary Edema
  2. Fibrosis (scarring) caused by inflammation
  3. Decreased surface area (emphysema)
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10
Q

Define FRC and be prepared to describe how it affects blood PaO2, PaCO2, and pH. What type of diseases would change FRC.

A

FRC = functional reserve capacity; the amount of air still left in the lungs after forced expiration

Increased FRC decreases O2 by diluting it

Increased FRC increases CO2 because of the difficulty in getting air out.

These diseases would change FRC:

Any of the airway diseases

  1. Asthma
  2. Bronchitis
  3. Emphysema
  4. Pneumonia
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11
Q

Define Ventilation/Perfusion mismatch and be prepare to describe generally how it affects blood PaO2, PaCO2, and pH. What type of diseases would cause a ventilation/perfusion mismatch

A

Ventilation/Perfusion mismatch:

High V/Q mismatch (>1): Ventilation is normal but diffusion is low

ex) pulmonary embolus

Low V/Q mismatch (

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12
Q

Define Right to Left shunt. Be prepare to describe generally how it affects blood PaO2, PaCO2, and pH. What type of diseases would cause a R -> L shunt.

A

Right to Left shunt –> when there is low PAO2 the vessels in the lungs are constricted to redirect blood flow to an area of the lungs with more perfusion ability
–> may lead to pulmonary HTN

Any disease that causes hypoxemia would a cause a right to left shunt

ex) pneumonia, atelectasis, completely obstructed airway

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13
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion abnormalities, FRC, V/Q mismatch and shunting

Chronic Bronchitis

A

Diagnosis: hypersecretion of mucus and chronic cough for 3 months out of the year for 2 consecutive yrs.

Etiology:

a. Inspired irritants increase mucus production and proliferation of mucus glands and goblet cells. Mucus is thicker, more tenacious, and difficult to clear.
b. Mucus provides an excellent medium for bacteria.
c. Ciliary function is impaired by inhaled irritants and infection

Pathophysiologies:

a. It first affects large airways and then smaller airways.
b. Chronic inflammation decreases airway diameter
c. Ciliary function is impaired
d. Early closing of airways during expiration = airtrapping and hyperinflation
e. Increased FRC, decreased PaO2 and increased PaCO2
f. hypoxemia, hypercapnia, and polycythemia
g. Pulmonary HTN due to hypoxemia and polycythemia
h. R heart hypertrophy and R heart failure (cor pulmonale)

Treatment:
a. Best treatment is prevention = bronchodilators, expectorants

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14
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting

Bronchiectasis

A

Definition: persistent abnormal dilation of the bronchi

Etiologies:

a. Mucus plugs
b. atelectasis
c. aspiration of foreign object (peanut)
d. infection as a child

Pathophysiology:

a. Formation of a pocket which is either cylindrical or saccular in shape
b. Injury to the ciliary membrane with fibrotic repair
c. Due to a&b the cavitation acts as a collection area for mucus which is difficult or impossible to clear
d. Mucus acts as a great breeding place for bacteria
e. Infectious bacteria digest the cavitation out further only deepening the pocket into surrounding lung tissue and blood vessels (hemoptysis)

Treatment:

a. Antibiotics and chest physiotherapy
b. O2 prn
c. This is not a curable disease, it is permanent and prevention is the best Tx

  • This would cause V/Q mismatch since it reduces VC and flow rates
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15
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting

Pneumonia

A

Definition: Accumulation of fluid in the lungs especially when caused by an infection

Etiologies: Lungs have come in direct contact with environment through inhaled air

a. Bacterial Infections
b. Viral Infections - less severe and self limiting
c. Aspiration

Pathophysiology:

a. Usually causes exudate from inflammation –> consolidation of infected lobe of the lung
b. Consolidation of infected lobe = R –> L shunt
c. Destroys cilia in airways of infected lobe, decreased clearance
d. Spreads to other lobes only worsening the R –> L shunt
e. Possible formation of abscess of lung

Treatment:

a. Rest and fluids
b. Chest physiotherapy
c. Antibiotic therapy

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16
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting

Pulmonary interstitial fibrosis

A

Pulmonary Interstitial Fibrosis will cause CHEST WALL RESTRICTION

Etiologies:

a. Idiopathic
b. Lupus
c. ARDS
d. Toxic inhalation
e. TB

  • This reduces VC due to loss of elasticity of lungs or the chest wall = V/Q mismatch
17
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting

Pneumothorax

A

Definition: presence of air/gas in the pleural space

  1. OPEN PNEUMOTHORAX - communicating air exchange between air in the pleural space and the outside environment

Etiology:
a. Rupture of or foreign object penetration of parietal pleura and chest wall (from stab, bullet wound, chest trauma)

Pathophysiology:

a. Breaks vacuum seal between visceral and parietal pleura
b. Lung collapses
c. Air is drawn into chest through wound upon inspiration
d. Air may be expelled through wound upon expiration
e. Other lung stays inflated and the mediastinum remains in place
f. Lose half of the O2 space = R –> L shunt

Tx: Cover wound on expiration and place a chest tube

  1. Tension PNEUMOTHORAX

Definition: rupture of parietal or visceral pleura; air can enter in inspiration but may not leave upon expiration - stays trapped in pleural cavity

Etiology:

a. Fracture of rib which tears visceral pleura
b. Traumatic rupture of visceral pleura or lung
c. Rupture of blebs on outside of lung
d. Puncture of chest wall where hole acts as a one way valve

Pathophysiology:

a. Air enters pleural space during inspiration but doesn’t escape during expiration; lung on affected side collapses
b. Increased pressure causes the mediastinum to move toward good lung
c. Good lung becomes compromised decreasing amount of air during inspiration
d. Compression of vessels in thoracic cavity

  • this would cause a V/Q perfusion problem and most likely a R –> L shunt

Tx: Insertion of chest tube to relieve pressure, insertion of bore needle, chest connection to a vaccum

  1. SPONTANEOUS PNEUMOTHORAX

Definition: occurs in fast growing tall, thin males and some females between 16-40; rupture of blebs due to thoracic cavity growing faster than lungs

Etiology:
a. Bleb rupture during sleep, rest, or exercise

Pathophysiology:
a. Partial collapse of lung leading to compression atelectasis

  • this would be a V/Q perfusion mismatch along with R–> L shunt
18
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

ARDS

A

Definition: acute lung inflammation and diffuse alveolar and capillary injury

Etiology:

a. Sepsis (G- bac) and multiple trauma
b. Smoke or noxious gas inhalation
c. O2 toxicity
d. Bypass surgery
e. Gastric aspiration
f. DIC
g. Anything that damages alveolar-capillary membrane and causes severe pulmonary edema

Pathophysiology:

a. Massive inflammatory response
b. Damage to capillary endothelial cells and increased capillary permeability
c. Platelet aggregation, serotonin, and thromboxane A2
d. Endotoxins released during sepsis
e. macrophages and neutrophils

  • Neutrophils - release inflammatory mediators that cause extensive damage
  • -> dramatically increases capillary permeability
  • -> proteins enter interstitial fluid and water follows
  • -> severe edema
  • Seratonin and thromboxane A2 cause vasoconstriction –> pulmonary HTN
    f. Sever edema, severe hypoxemia –> supplemental O2–> O2 toxicity
    g. Hypoxemia –> pulmonary vasoconstriction –> HTN
    h. Hyaline membrane forms –> barrier to O2 diffusion
    i. Surfactant production is impaired –> atelectasis and alveolar collapse
    j. Stiff noncompliant lungs
  • Severe v/q mismatch, severe r/L shunt
  • limited diffusion capacity, hypoxemia, hypercapnia
19
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

Pulmonary hypertension

A

Definition: normal mean arterial pulmonary pressure 15-18 mm Hg

HTN = 22-28 mm Hg

Etiology:
a. unknown
b. usually hits about 30-50 yrs of age
Secondary pulmonary HTN
c. chronic hypoxia
d. L heart disease
e. renal failure
f. over secretion of vasoconstrictors
g. Pulmonary disorders which cause reduction of the pulmonary capillary bed or constriction of the pulmonary aa. --> increasing pressure required to pump blood through
ex) pulmonary edema (compression of vessels), emphysema (destruction of capillaries), lung cancers (both compression and destruction), pulmonary artery vasoconstriction due to hypoxemia or acidosis

h. left heart failure –> pulmonary vascular congestion due to CAD or infarction
i. L –> R shunts

Pathophysiology:

a. Hypertrophy of pulmonary arterial smooth muscle –> chronic pulmonary HTN, decreased vessel compliance (recall this is facilitated by angiotensin II)
b. Pulmonary edema
c. R ventricular hypertrophy
d. Cor pulmonale

Tx: heart or lung transplant! also treat the underlying cause

  • This would involve R –> L shunt
20
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

Asthma

A

Definition: Inflammatory disease that results in hyper-reactive bronchial smooth mm. causing bronchial constriction

Etiology:

a. Activated by environmental antigens (pollens, dander, dust mite) –> Type I hypersensitivity response
b. Aspirin, air pollutants, cold dry air, exercise, stress (especially emotional)

Pathophysiology:

a. Antigen activates dendritic cells
b. Dendritic cells activate Th cells IL-4, IL-5…
c. IL-4 activates production of IgE from memory cells
d. Antibodies bound to mast cells bind to antigen
e. Mast cell degranulation
f. Releases histamines, leukotrienes, and bradykinins
g. Release chemotaxic factors for eosinophils and neutrophils

SECONDARY ATTACK (4-8 hrs later)

a. Eosinophil and Neutrophils
- release more inflammatory mediators
- protein stops cilia - disrupts mucosal cells
b. Prolonged inflammation –> hyper-reactive smooth mm.
c. Hypertrophy of smooth mm.
d. Air trapping and hyperinflation of the lungs

Tx: first and foremost –> remove causative agent
Steroid treatment to control inflammation
B agonists
Anticholinergic inhalers if B agonists are not tolerated well
Pt. education
Drug protocol based on asthma severity

21
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

Emphysema

A

Definition: enlargement of the acini (respiratory bronchioles) and rupture of the alveoli into eachother, forming large blebs and eventually cavities

Etiology:

a. a-antitrypsin deficiency: inhibits the action of protease enzymes; prevents destruction of the c.t. and proteins forming the alveolar walls and acini - particularly elastin
b. exogenous substances prevents the inhibition of proteases in the lungs (chemicals from smoking, accumulation of neutrophils - they release proteolytic enzymes)
c. Mechanical injury to alveoli to air-trapping and proteases

Pathophysiology:

a. Destruction of alveolar septa due to destruction of elastin
b. Reduction of lungs elastic recoil, increased FRC
c. Creation of bulla (large blebs in the lungs)
d. Reduction of the alveolar surface area of the lung for O2 and CO2 diffusion
e. Destruction and reduction of pulmonary capillaries –> pulmonary HTN –> cor pulmonale

Tx: Slow the progression of the disease - smoking cessation, supplemental O2 if hypoxemic, bronchodilating drugs and phrophylactic antibiotics

*FRC problem

22
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

cor pulmonale

A

Definition: pulmonary heart disease - right heart enlargement and failure secondary to pulmonary HTN

Etiology:
a. Pulmonary HTN

Pathophysiology:

a. Hypertrophy of the Right Heart –> hypertrophy cardiomyopathy
b. Dilation cardiomyopathy –> overdilation of right ventricle –> right heart failure
c. Failure occurs when pulmonary artery pressure = systemic arterial pressure

Tx: Decrease workload of the right heart

  1. venous vasodilation
  2. if possible, reversal of underlying problem
23
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

Atelectasis

A

Definition: collapse of lung tissue - usually referring to defuse alveolar collapse

Etiology:

a. Compression of lungs - external pressure, tumor, pneumothorax, fluid
b. Absorption atelectasis - remove or dissolving air out of alveoli
c. (b) combined with immobilization and shallow breathing ex) after surgery
d. Supplemental O2 increases risk, increased absorption rate
e. Plugging of airways due to bronchitis, asthma, mucus

Pathophysiology:

a. Blood absorbs the gases by diffusion, O2 quickly due to metabolic use
b. Alveoli slowly collapses overtime due to (a)
c. Low ventilation/perfusion mismatch
d. Hypoxemia due to (c)

Tx: Deep breathing, inflated other alveoli, air enters blocked alveoli through pores of Kohn
Early ambulation post surgery
If severe, mechanical ventilation

24
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

Hemothorax

A

Definition: presence of blood in the pleural space

Etiology: pleura is quite permeable and fluid will migrate as result of relative negative pressure of pleural space favors movement of fluid into space

a. Pulmonary edema due to increased capillary hydrostatic pressure (transudative effusion)
b. Pulmonary edema due to decrease plasma proteins (transudative effusion)
c. May occur as a result of pulmonary infection (increase capillary permeability) exudative effusion
d. May occur as result of malignancy

Pathophysiology:

a. Compression atelectasis similar to pneumothorax
b. Lung doesn’t collapse due to elastic recoil

  • V/Q mismatch

Tx: Small effusions reabsorb
Large effusions are aspirated through a needle inserted into the chest (called thoracentesis)

25
Q

Describe the etiologies, pathophysiologies, and general treatments for each of the pulmonary diseases listed below. Be prepared to describe each of these diseases in terms of diffusion
abnormalities, FRC, V/Q mismatch and shunting.

Pulmonary edema

A

Definition: Excess serum in the interstitial space between the alveolar capillary membrane (caused by excessive pulmonary capillary hydrostatic pressure, increased capillary permeability, decreased capillary osmotic pressure, blocked lymphatic drainage.)

Etiology:

a. Increased left heart filling pressure (MOST COMMON CAUSE)
- mitral stenosis, mitral regurgitation, L ventricular hypertrophy

This increases Cap Hydrostatic pressure and exceeds blood oncotic presure

> 20 mm Hg wedge pressure (normal is 8-10)

b. ARDS
- inhalation of toxic gases, sepsis, inflammation due to mechanical injury, aspiration pneumonia

Mechanism = increased capillary permeability, leaks out proteins –> loss of surfactant production

c. Compression of Lymphatic drainage
- edema, tumor, fibrocytic tissue

Mechanism = blocks drainage from interstitial spaces

Pathophysiology:

a. Hypoxia –> increased diffusion distance for O2
b. Increased work of breathing due to loss of lung compliance
c. affects PaCO2 only if sever

Tx: supplemental O2, diuretics, vasodilation (decrease L ventricular after load and L CHF)
drugs to increase cardiac contractility (digoxin)

26
Q

Define/Differentiate: Hypercapnea vs Hypoxia

A

Hypercapnea: PaCO2 > 40 mmHg caused by alveolar hypoventilation, decreased VE

  • -> decreased pH
  • -> hyperkalemia (low pH places K+ out of cell)
  • -> dysrythmias in heart
  • -> cerebral vasodilation (body’s response to decreased oxygen everywhere except lungs is to dilate) = increased intracranial pressure and edema only worsening the problem
  • -> leads to hypoxemia (increased CO2 decreases O2)

Hypoxia: lack of oxygen to the tissues

27
Q

Know and be able to identify Respiratory Failure in terms of blood PaO2, PaCO2, and blood
pH. Describe interventions of each type of failure.

A

Respiratory Failure: Inadequate gas exchange

PaCO2 > 50 mm Hg
Pa O2 50 mmHg) = mechanical ventilation

Hypoxemic respiratory failure (Pa CO2 > 50 mmHg) = mechanical ventilation and supplemental oxygen

28
Q

Be able to describe the three major components of O2 content and how O2 content differs
from PaO2

A

O2 content =

(Hb x SaO2 x 1.34) + (PaO2 x .003)

  1. Hb
  2. oxygen in blood bound to Hb
  3. partial pressure of arteriole oxygen
29
Q

Define atelectasis and describe the underlying mechanism that causes atelectasis. Identify who is at risk of developing atelectasis and which factors make increase that risk.

A

Atelectasis: collapse of lung tissue

Etiology:

a. Compression of lungs (fluid, tumor, pneumothorax)
b. Absorption atelectasis (removing or dissolving air out of alveoli)
c. (b) combined with immobility and shallow breathing after surgery
d. Supplemental O2 increases risk b/c of increased absorption rate
e. Plugging of airways due to asthma, bronchitis, mucus

Risk:

a. Those who are immobile
b. Those who just came out of surgery (shallow breaths)

30
Q

Describe the immediate danger of a tension pneumothorax

A

Air enters the pleural space during each inspiration but doesn’t leave upon expiration

This leads to a build up of air in the lungs causing hyperinflation

–> pushed the mediastinum toward the unaffected lung and ultimately will compromise it

31
Q

Be prepared to distinguish the differences between: Restrictive Pulmonary Disease vs Obstructive Pulmonary Disease

A

Restrictive Pulmonary Disease: Disease in which the VC is reduced due to loss of elasticity of lungs or chest wall

Obstructive Pulmonary Disease: Narrowing or occlusion of the airway obstructing airflow; usually indicated by an FEV1

Pathophysiology (15 decks)

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