Pulmonary Pathophysiology Flashcards

0
Q

What is the most common post-op complication and what is the rate of incidence?

A

Post-Op Pulm Dysfunction

Occurs between 6-60% of surgical population

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1
Q

What are the 4 categories of pulmonary pathophysiology?

A
  • Post-Op Pulm Dysfunction
  • Obstructive Lung Disease
  • Restrictive Lung Disease
  • Combination Obstructive/Restrictive Disease
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2
Q

What are some examples of Post-Op Pulm Dysfunction complications?

A
  • Atelectasis
  • Pneumonia
  • PE
  • Respiratory Failure
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3
Q

What are the risk factors for Post-Op Pulm Dysfunction?

A

*Operative Site (Thoracic and Upper Abd surgery causes splinting
because the Pt doesn’t want to take a tidal volume breath
secondary to pain)
*Surgical Duration (The longer the surgery, the greater the risk; dry
air will dry out Pulm system which causes stress to system)
*Pre-op Pulm Dysfunction
- Hx of dyspnea: pre-existing Dz, on home O2, SOB at rest
or on exertion
- Smoking: can’t clear secretions, damaged lungs can’t
protect themselves
- Advanced Age: widens the A/a gradient, destruction of
alveoli and capillaries, larger V/Q mismatch
- Obesity: decreases FRC

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4
Q

Describe what causes diaphragmatic dysfunction and what happens when this post-op pulm dysfunction occurs.

A

Diaphragmatic dysfunction occurs after upper abd and thoracic surgeries due to pain from the incision, inflammation and subsequent splinting.

The diaphragm doesn’t work as well because it bows up and, therefor, won’t allow for full lung expansion as a protective mechanism.

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5
Q

In upper abd and thoracic surgery, what is the decreased FRC post-op? When is this decrease at its maximum? How long does this decrease last?

A

FRC decreases 60-70%

It is maximal post-op day 1 (POD #1)

Decreases last 7-10 days

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6
Q

Pt’s s/p upper abd and thoracic surgeries have an increased work of breathing. What does this mean?

A

Pt’s use an increased amount of energy to breathe. This increases stress on the Pt and leads to an increased oxygen requirement.

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7
Q

What leads to decreased clearance of mucus in upper abd and thoracic surgeries? Why is this considered post-op pulm dynfunction?

A

The ETT itself, the dry air used to ventilate the Pt

Decreased clearance of mucus leads to pooling of mucus, which can result in infection, pneumonia and V/Q mismatch

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8
Q

Why does a Pt have decreased coughing after upper abd or thoracic surgery?

A

pain protection

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9
Q

What post-op pulm dysfunctions would you expect in upper abd and thoracic surgeries?

A
  • Diaphragmatic dysfunction
  • Decreased FRC
  • Increased work of breathing
  • Decreased clearance of mucus
  • Decreased coughing
  • Pulm shunting
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10
Q

Describe pulmonary shunting

A

The Pt has unventilated alveoli, meaning that blood passes by without ‘picking up’ oxygen. This leads to hypoxic vasoconstriction, which acts as a protective mechanism (though can’t completely protect the pulm system) and eventually leads to increased right ventricle pressure, increased pulmonary vascular resistance and, ultimately, (short term or longterm) pulmonary HTN.

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11
Q

What are the Co-existing established risks for post-op pulmonary complications?

A
  • Smoking
  • Obstructive lung disease (COPD, poorly controlled asthma)
  • Malnutrition
  • Chronic respiratory tract infections
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12
Q

What are the co-existing potential risks for post-op pulmonary complications?

A
  • Age
  • Obesity
  • Stable or Mild Asthma
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13
Q

What are the surgery associated established risks for post-op pulmonary complications?

A

*Surgery Type (Thoracic/Upper Abd > Lower Abd > Peripheral)
*Type of incision (Thoracotomy ie between ribs > Sternotomy ie
down sternum)
*Type of anesthesia (General > Neuraxial/Regional, even in
peripheral surgeries)
*Duration of surgery (The longer the surgery, the great the risk)

Note: if a lung is collapsed during the proceedure (1 lung ventilation), there is an even greater risk to the pulmonary system)

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14
Q

What are the surgery associated potential risk levels for post-op pulmonary complications during a thoracotomy?

A

The risk level increases according to how the surgical site is accessed

Posteriolateral thoracotomy > muscles-sparing thoracotomy > thoroscopic

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15
Q

Describe the difference between obstructive lung disease and restrictive lung disease

A

In OBSTRUCTIVE lung disease, the lungs are hyper-inflated (overextended) which leads to a greater residual volume/FRC. It is harder for the Pt to exhale and takes greater work and time to move air out of the lungs.

In RESTRICTIVE lung disease, lung volumes are decreased due to a limitation in how well the lungs can expand. It takes more work and energy to inhale.

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16
Q

What are examples of obstructive lung disease?

A
  • Asthma (from mild to severe, though can out grow)

* COPD (aka emphysema, progressive, usually related to environmental exposure)

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17
Q

True or False: Too light of an anesthetic during intubation can lead to a reaction from hypersensitive airways.

A

True.
Smooth bronchial muscles will spasm/contract/constrict leading to narrowing of the airways, which is the 1st phase of the asthmatic response.

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18
Q

True or False: An asthmatic has an abnormal airway, which leads to hypersensitivity.

A

FALSE.
An asthmatic does have a hypersensitive airway, but their airway is normal until the hypersensitivity is triggered by a stimulus. The stimulus can be internal (mismatch between sympathetic/parasympathetic state), external or environmental

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19
Q

Describe the physiological changes that occur during acute asthma exacerbation

A

Bronchial Muscle Hyperactivity -> Airflow Limitations -> Recruitment of Inflammatory Cells and Mediators -> Continued and Worsening Bronchospams -> Alveolar Fluid Extravisation

Note: this is another way he described it -
A Pt’s bronchioles respond to a stimulus -> bronchial smooth mucles spasm leading to contraction/constriction and narrowing of the airways -> inflammatory cells act as inflammatory mediators -> hyper secretory response occurs -> mucus fills Pt’s airway -> more bronchospasm occurs in already narrowed airways

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20
Q

What are the primary and secondary phases of an asthma attack, respectively?

A

primary: bronchoconstriction
secondary: inflammation

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21
Q

What are potential treatments for asthma?

A
  • Bronchodilators
  • Steriods
  • Anticholinergics
  • Methylxanthines
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22
Q

What are 2 examples of Bronchodilators?

A
  • Beta2-agonists (Albuterol)

* Epinephrine

23
Q

Why is epinephrine used to treat asthma?

A

Epinephrine has beta2-agonist properties and limits mast cell degranulation

24
Q

Why are beta2-agonists used to treat asthma?

A

They act on the catecholamine receptors on the bronchial smooth muscle

25
Q

Why are steroids used to treat asthma? When/how are they normally used.

A

Steroids help blunt the secondary inflammatory response in asthma.

Steroids should be used intravenously for acute asthma exacerbation. Otherwise, steroids are primarily used as a daily maintenance treatment in the form of inhalational steroids. This way, they is much less systemic absorption of the steroids and little to no negative side effects from being on long term steroid therapy.

26
Q

Give an example of a Methylxanthine

A

Caffeine (which can act as a bronchodilator)

27
Q

What should you ask an asthmatic pre-operatively?

A

*Severity of Asthma (most recent attack, # of attacks, resolution of
attacks)
*Clinical Hx (steroid/inhaler use, intubation Hx, currently wheezing, *Exacerbating factors (smoking, allergens, exercise)

Note: you should also determine baseline peak flow values

28
Q

What should you consider when pre-oping an asthmatic?

A

*Is the Pt optimized? How? (Bronchodilators, Glucocorticoids,
Supplemental Oxygen)
*PFTs (helps assess optimization, not very useful for Pt’s on a
chronic therapy regimine)
*Should the Pt be sedated to decrease anxiety (anxiety triggers
bronchospastic response)
*Does the Pt need a stress dose of steroids (if the Pt recently
finished IV or PO steroids, they might need steroids because
steroids cause adrenal gland suppression so the Pt might not
be able to produce steroids peri-operatively. Natural steroids
are highly important in stressful situations, like surgery).

29
Q

What is the most critical moment for an asthmatic during surgery?

A

Instrumentation of the airway

Note: you might also want to consider deep extubation to avoid coughing or bucking on the tube, which can also cause bronchospasm

30
Q

How does intraoperative wheezing reflected in monitors?

A

*Increased peak airway pressures, but plateau pressures remain
the same
*Decreased exhaled tidal volumes
*Slow rise on capnogram tracing (shark fin)

31
Q

What are non-asthmatic causes of intraoperative wheezing?

A
  • Main stem intubation
  • Light anesthetic (coughing/bucking)
  • Allergic response
  • Obstructed ETT
  • Excessive secretions
  • Forceful expiration (light anesthesia)
  • Pulmonary edema
  • PE
  • PTX
32
Q

What is the most common pulmonary disorder seen in the OR?

A

COPD

33
Q

Describe the physiological changes that lead to COPD

A

irritants get into lung parenchyma (most commonly from environmental exposure to toxins/smoking) -> cilia get bogged down with particulate matter -> epithelial cells are damaged -> inflammatory response incited at the same time (cellular mediated and humoral inflammatory response with the release of inflammatory mediators) -> fibroblast proliferation (scar tissue formed)-> leads to destruction of alveoli/alveolar walls -> alveoli merge into ‘mega’ alveoli (blebs) -> destruction of wall between alveoli and capillary beds -> destruction of capillary beds themselves (ie alveolar/capillary units get destroyed) -> progressively worsening gas exchange -> chronic hypoxemia, hyper secretion of mucus throughout pulmonary system

34
Q

Why is it harder for COPD Pt’s to exhale?

A

lungs lose elastic recoil

35
Q

What pathophysiological changes occur as a result of COPD?

A
  • Pt has increased areas of intrapulmonary shunt
  • Pt has increased areas of dead space
  • Capillary destruction
  • Alveolar destruction (A/a gradient widens)
  • Bronchial component: increased secretions, inflammatory response, reactive component
36
Q

What happens as a result of capillary destruction and chronic hypoxemia?

A

increased pulmonary vascular resistance -> increased stress on right heart -> problems with perfusion of the lungs -> right heart strain (cor pulmonale) -> right heart failure

37
Q

How is chronic bronchitis diagnosed?

A

Pt must have a chronic, productive cough most days, lasting for at least 3 months at a time for a period of 2 years

38
Q

A normal I:E ratio is 1:2 or 1:2.5, what is the I:E ratio in COPD?

A

1:3 - 1:4

39
Q

What is cor pulmonale?

A

heart failure that develops as a result of chronic lung disease

40
Q

What results from chronic hypoxemia?

A

*Erythrocytosis (increased RBC/Hgb production, Hct well into 40s
and 50s will give you an idea about chronic hypoxia)
*Pulmonary HTN
*Cor pulmonale
*CO2 retention (Respiratory acidosis will lead to metabolic
alkalosis so a paO2 of 50 and paCO2 of 50 will be accompanied
with an increased HCO3 in high 20s-30s, ie compensated
respiratory acidosis)
*Blunted ventilatory drive (higher baseline CO2 levels, the blunting
effect can be intensified with narcotics and anesthetics, which is
why these Pt’s have a greater incidence of remaining intubated_

41
Q

What things should be considered pre-operatively for COPD Pt’s?

A
  • Recent changes in a Pt’s symptoms (means Pt isn’t optimized)
  • CXR (chronic PNA? chronic bronchitis? cor pulmonale?)
  • PFTs
  • Baseline ABG (don’t want to ‘over optimize’ Pt)
  • Cardio evaluation (echo?)
  • Infection control (ABx?)
  • Bronchdilators
  • Steroids
  • Anticholingergics (decrease secretions?)
42
Q

When should a Pt stop smoking to optimize surgical conditions?

A

6-8 weeks prior to surgery, this will help decrease secretions

any sooner (8+weeks) leads to increased secretions as a hyper response

43
Q

How do you Dx a bronchospasm in a COPD Pt?

A

Chest Auscultation

44
Q

How do you Dx Atelectatsis in a COPD Pt?

A

CXR, listen for decreased breath sounds

45
Q

How do you Dx Infection in a COPD Pt?

A

Symptoms, Cultures

46
Q

How do you Dx Pulmonary Edema in a COPD Pt?

A

CXR, listen to lungs for crackles

47
Q

What can you do intervention wise during the preoperative period for a COPD Pt?

A

*Correct hypoexemia (Is there anything new causing the
underlying condition?)
*Correct Bronchospasm
*Mobilize secretions (help the Pt clear secretions)
*Reduce secretions
*Control infection

48
Q

Essentially, how do Pt’s with restrictive pulmonary disease decrease the work of breathing?

A

Pt’s take smaller tidal volume breaths at a more rapid rate. This increases the effectiveness of ventilation against stiffer, less compliant lungs.

49
Q

What are characteristics of restrictive pulmonary disease?

A

*Decreased lung compliance (Lungs aren’t as easy to distend.
They have a somewhat increased elasticity as a result of lungs
wanting to spring back to a smaller volume state.)
*Reduced lung volumes (do to the decreased compliance)
*Normal expiratory flows (unlike obstructive disease)
*Increased work of breathing
*Maintenance of gas exchange (capillary/alveolar membrane
remains intact, again unlike obstructive disease)

50
Q

Why is the increased work of breathing different in restrictive lung disease compared to the increased work of breathing in obstructive lung disease?

A

In RESTRICTIVE lung disease, this is do to resistance to lung expansion (decrease in compliance).

In OBSTRUCTIVE lung disease, this is do to a resistance of air flow (decrease in expiratory flow).

51
Q

Why are spinal deformities, such as kyphosis, considered a restrictive lung disease?

A

Kyphosis (osteoporosis to the point of compression Fx’s in the spine) and other spinal deformities limit the ability of a Pt’s lungs to expand because the Pt is hunched over, ie *chest excursion is limited. The parenchyma/lungs themselves are (usually) ok.

*Note: Normal chest wall mobility is important for effective lung expansion and subsequent ventilation. Chest wall mobility is often assessed by measuring chest excursion, the difference between chest girth at maximal inhalation and maximal exhalation. Chest excursion measurements are used to evaluate the effect that restrictive pulmonary diseases, such as ankylosing spondylitis, idiopathic scoliosis, muscular dystrophy, spinal cord injuries, and chronic obstructive pulmonary disease, have on chest wall range of motion.1-14 In addition, chest excursion can be used as an indicator of respiratory muscle function (recruitment and/ or strength) in patients with neuromuscular disease.15 Clinically, chest excursion measurements are used to evaluate a patient’s baseline status, treatment effectiveness, and progression of disease with regards to chest wall mobility and respiratory muscle function.

52
Q

Why is a Pt with burns circumventing the chest considered to have restrictive lung disease?

A

Severe burns around the chest lead to immediate eschar (slough or piece of dead tissue that is cast off from the surface of the skin particularly after a burn injury). Therefore, burn tissue is much more rigid and restrictive. An escharotomy is performed to free the chest.

53
Q

List the 8 examples of restrictive pulmonary disease given in the lecture.

A

*Pulmonary edema (interstitial fluid stiffens lungs)
*PNA
*Aspiration (can also lead to inflammation)
*Severe chest wall deformities
*Cystic fibrosis
*Pulmonary fibrosis
*Interstitial lung disease
*Severe abd distention (sever ascites, abd pathologies, intestinal
swelling, air in stomach in tiny infants do to ventilation)

54
Q

Compare the forced expiratory volume in normal, obstructive lung diseased and restrictive lung diseased Pt’s.

A

In NORMAL Pt’s FEV should be 70%, ie 70% of the lung volume air should be exhaled in the 1st second.

In OBSTRUCTIVE diseased Pt’s, FEV s, FEV is less than 70%