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VF1 - Block 3 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Mechanism of Action of anti-cholinergics

A
  • Block cholinergic receptors –> smooth muscle relaxation –> bronchodilation
  • Block cholinergic receptors –> decreased mucus production
  • Recall: acetylcholine = parasympathetic = bronchoconstriction
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2
Q

Mechanism of Action of Beta-agonists

A

Bind B2 receptors –> smooth muscle relaxation –> bronchodilation

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3
Q

SABAs

A

albuterol terbutraline

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4
Q

LABAs

A

salmeterol formoterol

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5
Q

Why use corticosteroids with B-agonists?

A

Long-term use of B-agonists causes downregulation of B-receptors. Corticosteroids cause up-regulation of B-receptors, so when you have an acute attack, corticosteroids make your SABA more effective.

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6
Q

Side Effects of B-2 agonists

A
  • Muscle tremor (skeletal muscle β2 receptors) particularly in elderly
  • Tachycardia (Atrial β2 receptors, myocardial β1 receptors at high doses)
  • Hypokalemia (K+ flux into skeletal muscle) Potentially serious in certain situations but rarely observed with inhaled forms
  • Ventilation perfusion mismatch (shunting of blood to poorly ventilated areas) usually not a problem although significant drop in paO2 can occur in COPD
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7
Q

anti-cholinergic drugs

A
  • ipatropium
  • tiotropium
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8
Q

Inhaled corticosteroid drugs

A
  • Beclomethasone
  • Fluticasone
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9
Q

Systemoic corticosteroid drugs

A
  • Prednisone
  • Hydrocortisone
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10
Q

Treatment of choice for asthma

A

Inhaled B-2 agonists

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11
Q

Benefit of inhaled vs. oral B-2 agonists

A
  • Inhaled minimizes systemic exposure –> minimizes side effects
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12
Q

Anti-cholinergic therapeutic considerations for asthma

A
  • Often used in patients who don’t respond well to B2 agonists
    • older patients who have a tremor from B2 agonists
  • Less effective than B2 agonists
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13
Q

Anti-cholinergic therapeutic considerations for COPD

A
  • These can be more effective than B2 agonists for COPD treatment
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14
Q

Corticosteroids mechanism of action

A
  • Regulate transcription factors = broad effects
  • Delayed response due to changes in transcription factors
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15
Q

What class of drug is used to induce pulmonary surfactant production?

A
  • Corticosteroids
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16
Q

Effects of corticosteroids

A
  • Suppress inflammatory response
  • Suppress mucus secretions
  • Increase B2 receptors on cell surface, which makes B2 agonists more effective when used in conjunction
  • Overall they don’t directly impact smooth muscle contraction but they do impact hyperresponsiveness
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17
Q

Inhaled corticosteroid drugs

A
  • Beclomethasone
  • Fluticasone
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18
Q

Systemic corticosteroid drugs

A
  • Prednisone
  • Hydrocortisone
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19
Q

When are inhaled corticosteroids used?

A
  • In all forms of asthma now
  • Recently new guidelines say that inhaled corticosteroids should be used in conjunction with SABA even for mild asthma
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20
Q

Inhaled corticosteroids used for COPD or CF?

A
  • Not really
  • Resistance to corticosteroids is pretty common for both COPD and CF
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21
Q

When are systemic corticosteroids used?

A
  • Acute exacerbations of asthma
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22
Q

Side effects of inhaled corticosteroids

A
  • dysphonia (problems w/ your voice)
  • oral candidiasis (i.e. flush)
  • cough
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23
Q

side effects of systemic corticosteroids

A
  • much worse than inhaled corticosteroids
  • Most significant: adrenal suppression and insufficiency
    • Due to exogenous corticosteroids
    • SLOW TAPER is critical for these patients
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24
Q

Anti-IgE receptor drug

A
  • Omalizumab
  • Used for asthma
  • Prevents IgE from binding to mast cell –> prevents degranulation and release of inflammatory cytokines
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25
Q

Anti-IL-5 antibody drugs

A
  • Mepolizumab
  • Reslizumab
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26
Q

Delivery of omalizumab

A

SubQ injection every 2-4 weeks

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27
Q

Main side effect of biologics

A
  • Immune response to the monoclonal Antibody itself
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28
Q

Indication for anti IL-5 antibody drugs

A
  • Eosinophilic asthma
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29
Q

Leukotriene Receptor antagonist drugs

A
  • Montelukast
  • Zafirlukast
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30
Q

5-lipoxygenase inhibitor drug(s)

A
  • Zileuton
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31
Q

Mechanism of action of leukotriene modifier drugs

A
  • Leukotriene is an inflammatory molecule released during an immune response
  • The leukotriene receptor antagonists block binding of leukotriene
  • The 5-lipoxygenase inhibitor blocks the enzyme (lipoxygenase) that actually synthesizes leukotriene
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32
Q

Therapeutic uses of leukotriene modifiers

A
  • Particularly effective in aspirin-induced asthma
  • Not effective for COPD
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33
Q

Side effects of leukotriene modifiers

A
  • RARE: liver toxicity
  • Generally safe and well tolerated
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34
Q

Bronchiectasis definition

A
  • pathologic enlargement of the airways
  • Result: fill with sputum and secretions
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35
Q

Bronchiectasis vs. bronchitis

A
  • Both see chronic coughing and sputum production
  • Bronchiectasis has PURULENT (infected) sputum
  • Bronchiectasis recurs while bronchitis resolves with treatment
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36
Q

CXR of bronchiectasis

A
  • Fibrosis –> thickenings on Xray
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37
Q

CT-scan of bronchiectasis

A
  • Diagnostic test
  • See sacs of air = enlarged airways
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38
Q

Traction bronchiectasis

A
  • Pulmonary fibrosis –> scarring –> airways stay opened
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39
Q

Pathogenesis of bronchiectasis

A
  • Most common cause: infection
  • TB can cause it
  • Childhood injury to airway and resulting abnormal growth can cause it
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40
Q

Result of bronchiectasis

A
  • Impaired secretion clearance
  • Chronic infection
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41
Q

Pathogenesis of CF

A
  • Autosomal recessive
  • CFTR mutation –> dysfunctional CFTR protein
  • CFTR protein = channel protein for chloride
  • Dysfunctional protein –> low chloride –> low water –> thickened mucus –> cilia cannot clear mucus –> infections
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42
Q

Most common bacterial infections in CF patients

A
  • Staph
  • Pseudomonas
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43
Q

Clinical Progression of CF

A
  • Normal lungs at birth
  • slow recovery from respiratory infections
  • Chronic infection –> bronchiectasis (chronic inflammation + enlarged airways filled w/ mucus)
  • Deterioration of pulmonary function tests
    • Obstructive disease
  • ​Episodes of exacerbations
  • Eventual respiratory failure
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44
Q

Most common mutation in CF

A
  • F508del
  • Causes misfolded protein that does not get trafficked to cell surface
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45
Q

Diagnosis of CF

A
  • Sweat test
    • High chloride and sodium in sweat b/c dysfunctional protein means chloride cannot get out but it also cannot get reabsorbed
  • Genotyping
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46
Q

G551D mutation

A
  • Another common mutation in CF
  • protein is made and gets to the cell membrane, but the ion channel doesn’t work b/c the gate won’t open
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47
Q

Medications used to treat CF

A
  • DNAse
    • DNA makes up majority of the thick mucus secretions
    • DNAse chews up the secretions to make it easier to clear
  • Nebulized saline
    • Pulls fluid into the airway –> loosens mucus secretions
  • Inhaled antibiotics
    • Especially to treat exacerbations
  • Ivacaftor
    • Designed to treat G551D mutation, which is only about 5% of patients
  • Elexacaftor/Texacaftor/Ivacaftor
    • Targets F508del and G551D mutations
    • Approved October 2019
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48
Q

Mechanical treatments for CF

A
  • Percussion
  • Vests
  • Blow into device that causes vibrations
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49
Q

Ultimate cure for CF

A
  • Lung transplants
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50
Q

Pathophysiology of a small Pulmonary Embolism

A
  • Increased dead space
  • Normally this would increase pCO2, but the patient compensates
  • Compensatory response is to increase respiratory rate, so what you end up seeing is a low pCO2 and respiratory alkalosis.
  • You still see low pO2 due to hypoxemia
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51
Q

Cause of hypoxemia in small PE

A
  • V/Q mismatch
    • Ventilation but no perfusion
      • Blood flow is diverted to other areas of the lung
  • Reduced cardiac output
    • You’ll see a reduced MVO2 b/c lower CO –> more oxygen extraction at the level of the tissues
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52
Q

Pathophysiology of large PE

A
  • LARGE PE can result in build up of lactic acidosis due to oxygen starvation in tissues
  • You’ll see a metabolic acidosis in this case
  • Large emboli –> Increased PVR (due to toxic mediators + hypoxemia causes vasoconstriction) –> right ventricular failure –> inadequate left ventricular filling –> decreased cardiac output –> hypotension and shock.
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53
Q

Infarct physiology of PE

A
  • Pulmonary Infarct may occur w/ PE
  • See these things potentially
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54
Q

Common Findings with PE

A
  • Respiratory alkalosis – due to V/Q mismatch and increased respiratory rate to compensate
  • Respiratory acidosis – due to LARGE PE à hypotension and shock
  • Calf pain/swelling – most statistically significant
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55
Q

Risk Factors for PE

A
  • Virchow’s Triad
    • Stagnant blood
    • Abnormal coagulation
    • Tissue injury
  • Recent travel
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56
Q

Most important sign for PE

A
  • Calf swelling/tenderness
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57
Q

Common symptoms for PE

A
  • Dyspnea
  • Pleuritic chest pain
  • Hemoptysis
  • Leg swelling/pain
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58
Q

Common Signs for PE

A
  • Tachypnea
  • Low grade fever
  • Friction Rub
  • Increased P2
  • Rales
  • Wheezes
  • Calf swelling/tenderness
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59
Q

First test when you suspect PE

A
  • Doppler ultrasound
  • if you see a clot, then you assume the lung issues are PE
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60
Q

Wells score

A
  • Used to categorize people’s risk for PE
  • A score above a 4 is high risk
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61
Q

D-dimer test

A
  • Used when you suspect PE
  • If positive, you do a CT angiography
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62
Q

V/Q scan and utility

A
  • Used when suspected PE
  • Inject radiolabeled albumin
  • The albumin will get caught where the clot is and you’ll be able to visualize where blood flow is and is not
  • High clinical suspicion + abnormal V/Q = VERY high likelihood of PE
  • Low clinical suspicion + normal V/Q = VERY high likelihood it is NOT a PE
  • Anything in the middle = the test is not very useful/predictive
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63
Q

Treatment of PE

A
  • Hemodynamically unstable: heparin + thrombolytic + coumadin
  • Hemodynamically stable: heparin + coumadin
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64
Q

Most common thrombolytics for PE

A
  • tPA (tissue plasminogen activator)
  • urokinase
  • Streptokinase (less commonly)
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65
Q

What do we do for PE patients who cannot tolerate a clot buster?

A
  • Insert filter into inferior vena cava to catch clots
  • Problem: this is associated with increased risk of lower extremity thrombosis
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66
Q

What do we do re: long-term treatment for PE?

A
  • Treat with warfarin for 3 – 6 months IF THEY HAVE A DEFINED REVERSIBLE RISK FACTOR.
  • If you cannot find their risk factor, it’s recommended they stay on life-long anticoagulation
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67
Q

Define asthma

A
  • Airway inflammation
  • Bronchial hyperresponsiveness
  • Obstructive lung disease
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68
Q

Pathophysiology of asthma

A
  • Environmental trigger –> inflammatory response
  • Two responses to this inflammatory response that narrow the airways:
    • Bronchospasm of smooth muscle around bronchioles
    • Increased mucus secretion
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69
Q

Pathologic changes in the airways in asthma

A
  • More goblet cells in epithelial lining –> increased mucus secretions
  • Sub-basement membrane is thickened
  • More immune cells present
  • In REALLY bad cases of asthma, you’ll see mucus plugs, REALLY thick layer of smooth muscle
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70
Q

Primary asthma symptoms

A
  • Coughing
  • Wheezing
  • Shortness of breath
  • Tightness in the chest
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71
Q

Diagnosis of asthma

A
  • Episodic symptoms are present
  • Airflow obstruction is present
  • Exclude alternative diagnoses
    • COPD
    • vocal cord dysfunction
    • allergic bronchopulmonary aspergillosis
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72
Q

Tests to diagnose asthma

A
  • Physical exam
    • Wheezing in lung sounds
    • Decreased breath sounds is a REALLY bad sign b/c they have progressed beyond just wheezing and now they’re not moving any air basically at all
  • Spirometry
    • See scooped expiratory curve on Volume-Flow loop
    • Decreased FVC and FEV1
  • Methacholine Testing
    • Good test to rule OUT asthma
      • If pre-test probability for asthma is really high, a negative methacholine doesn’t help that much
      • If pre-test probability for asthma is quite low, a negative test makes it really unlikely that the person has asthma
    • Checks to see whether patient has hyperresponsiveness
    • Method: Have them inhale methacholine to induce bronchospasm. If the FEV1 drops 20%, it indicates hyperresponsiveness. (Most people will have a small reaction to methacholine but not this much.)
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73
Q

How to assess severity of asthma?

A
  • Frequency of exacerbation
    • Night-time symptoms?
  • Severity of symptoms
    • Impairing daily function?
  • Frequency of medication use
  • Frequency of hospital visits
  • Spirometric readings – how bad is FEV1/FVC and Peak Expiratory Flow Rate
    • Severe asthma will show Decreased FEV1, or PEF <40%
    • Life Threating asthma can show same markers at <25%
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74
Q

Basic pharmacologic approach to treating asthma

A
  • Mild may just need a short-acting bronchodilator (albuterol)
  • Next steps: inhaled corticosteroids, long acting bronchodilators, biologics, oral corticosteroids
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75
Q

pharmacologic properties of main asthma medications

A
  • Albuterol = beta-agonist = bronchodilator
  • Corticosteroids = TF activation that is widespread = anti-inflammatory
  • Biologics = bind to immune antibodies like IgE that causes release of all sorts of inflammatory cytokines
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76
Q

Factors that can worsen asthma

A

house dust mite allergy

tobacco smoke

cats

seasonal allergens

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77
Q

Markers of acute asthma

A
  • Difficulty speaking in full sentences
  • Quiet chest (when they have progressed beyond wheezing). This is a BAD sign.
  • paCO2 > 45 mmHg
  • Oxygen Sat < 90%
  • FEV1 or PEF < 40%
    • Life-threatning asthma can show these parameters at less than 25%
  • Confusion/coma
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78
Q

Definition of COPD

A
  • A common, preventable, and treatable disease characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases
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79
Q

Prevalence of COPD

A
  • 20% of COPD is NOT smoking related
  • Highest prevalence in rural areas
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80
Q

How to diagnose COPD

A
  1. Symptoms
  2. Risk factors
  3. Spirometry
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81
Q

COPD symptoms

A

dyspnea

chronic cough

sputum

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82
Q

spirometry in COPD

A

FEV1/FVC < 70%

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83
Q

COPD risk factors

A
  • SMOKING
  • Indoor cooking w/ coal or wood
  • childhood respiratory infections
  • alpha-1-antitrypsin deficiency
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84
Q

Two forms of COPD

A
  • chronic bronchitis
  • emphysema
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85
Q

Pathophysiology of chronic bronchitis

A
  • Problem with the airway
  • Chronic inflammation –> mucus hypersecretion –> airway obstruction
    • See increased number of goblet cells
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86
Q

clinical diagnosis for chronic bronchitis

A
  • chronic productive cough for 3 months in each of 2 successive years
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87
Q

Pathophysiology of emphysema

A
  • Toxin (i.e. cigarette smoke) –> neutrophil degranulation –> release of elastase (protease that breaks down elastin)
  • Cigarette smoke also decreases alpha-1-antitrypsin, a protective antiprotease
  • Together results in destructino of elastin –> permanent enlargement of air spaces = floppy balloon
  • Results in hyperinflation, air trapping, imparired gas exchange
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88
Q

spirometry readings in COPD

A
  • Decreased FEV1/FVC
  • Increased TLC (due to air trapping)
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89
Q

Blue Bloater presentation

A
  • chronic bronchitis
  • V/Q mismatch
  • Cyanosis
  • Normal DLCO
90
Q

Pink Puffer presentation

A
  • emphysema
  • V/Q stays about normal
    • Lung tissue and capillaries are both destroyed
  • Air trapping
    • Increased residual volume
    • Increased TLC
    • Decreased Vital Capacity
  • Pursed lip breathing
  • barrel chest
  • Tripod position
  • Decreased DLCO
91
Q

Common causes of COPD Exacerbations

A
  • Pulmonary Embolism
  • Infections (bacterial or viral)
92
Q

Chronic bronchitis vs. asthma vs. emphysema

A
93
Q

alpha-1-antitrypsin deficiency

A
  • alpha-1-antitrypsin is a protective antiprotease
  • Deficiency –> breakdown of elastin in the lungs –> emphysema
  • Affects both lungs and liver
  • Inherited disorder
  • Shows panacinar emphysema rather than centriacinar –> lower lobes more likely to be affected
94
Q

Centriacinar vs. panacinar emphysema

A
  • Centriacinar is the most common and it just affects proximal alveoli
    • Usually smoking related
    • Usually upper lobes affected more
  • Panacinar is where the whole acinus is affected
    • Usually alpha-1-antitrypsin deficiency related
    • Usually lower lungs affected more
95
Q

Clinical Management of COPD

A
  • STOP SMOKING
  • Medications
    • B2 agonists (SABA, LABA)
      • As needed
    • Muscarinic antagonists (SAMA, LAMA)
      • Maintenance
    • Inhaled corticosteroids
      • Maintenance
96
Q

Clinical Management of COPD exacerbations

A
  • All the normal medications plus…
  • Roflumilast for chronic bronchitis
  • Azithromycin
  • Oral steroids (prednisone)
  • ***Supplemental O2 shown to improve mortality in COPD***
  • BIPAP
97
Q

Surgeries for advanced COPD

A
  • Transplant
  • Lung volume reduction surgery
  • bronchoscopic lung volume reduction
98
Q

Pneumonia CXR findings

A
  • Typically not bilateral
99
Q

CXR right upper lobe pneumonia

A
100
Q

CXR right middle and lower lobe pneumonia

A
101
Q

Definition of pneumonia

A
  • An acute infection of the pulmonary parenchyma that is associated with at least some symptoms of acute infection
  • Accompanied by the presence of an acute infiltrate on CXR or auscultatory findings consistent with pneumonia
102
Q

Risk factors for pneumonia

A
  • Smoking
  • Chronic bronchitis
  • HOSPITALIZATION
  • Feeding tube/ventilator
  • Anything making you aspirate more
    • alcohol
    • CNS depressant drugs
    • CNS diseases
    • Nasogastric tubes
103
Q

Most common diseases underlying pneumonia

A
  1. immunosuppression
  2. Alcohol abuse
  3. COPD
104
Q

Most common organism responsible for community acquired pneumonia

A

Strep pneumoniae

105
Q

Bulging fissures on X Ray plus currant jelly sputum

A
  • Klebsiella pneumoniae causing pneumonia
106
Q

Extremely virulent organism causing pneumonia. It can cause cavitary, necrotizing pneumonia.

A

Staphlococcus aureus

107
Q

Multi-drug resistant organism causing pneumonia. Also commonly seen in CF patients.

A

Pseudomonas

108
Q

Mucor

A

A fungus that causes really bad pneumonia

109
Q

Symptoms for pneumonia

A
  • Fever
  • Cough
  • Blood tinged sputum
  • Pleuritic chest pain
  • Shortness of breath
  • Fatigue
  • Nausea, diarrhea
110
Q

Diagnostic tests for pneumonia

A
  • Sputum gram stain and culture
  • Procalcitonin levels
    • bacterial = high procalcitonin
    • viral = low procalcitonin
  • CXR
111
Q

Procalcitonin levels

A
  • Test often used in diagnostics of pneumonia
  • Tells you whether pneumonia is bacterial or viral
  • Can help you decide whether to use antibiotics and when to stop using antibiotics
112
Q

Causes of Pericarditis

A
  • Infection
    • Most commonly it’s viral
  • Non-infectious
    • 3-4 days after an MI
    • Trauma
    • After radiation
    • Cancer
113
Q

Clinical features of pericarditis

A
  • SHARP chest pain
    • Worse when lying down
  • SOB, cough, hiccups
  • Friction rub on exam
  • Fever, fatigue, malaise
  • CXR often normal
114
Q

Diagnosis of pericarditis

A
  • EKG findings
  • Echo
    • Visualize effusions
  • Pericardiocentesis
    • Sample fluid in case of infection
  • CXR usually normal
115
Q

EKG findings with pericarditis

A
  • STEMI but it’s CONCAVE
    • STEMI in MI shows tombstones
  • Diffuse ST-elevations
    • MI shows ST-elevation on just a few leads
  • PR depression
  • T-wave peaking
116
Q

Tx for pericarditis

A
  • NSAIDs
117
Q

Pericardial effusion causes

A
  • Pericarditis
  • Free wall rupture –> death
118
Q

Signs/symptoms of pericardial effusion

A
  • Friction rub
  • If really large, may hear muffled heart sounds due to fluid
  • Narrow pulse pressure
    • Due to decreased SV b/c of problems with filling the heart
119
Q

Diagnosis of pericardial effusion

A
  • CXR
    • enlarged cardiac silhouette
  • EKG
    • Electrical alternans
    • Low-voltage EKG
120
Q

Electrical alternans

A
  • See variation in QRS complex from beat to beat
  • Result of pericardial effusion
121
Q

Tx of pericardial effusion

A
  • Treat cause of pericarditis
  • Pericardiocentesis to pull fluid off
122
Q

Causes of cardiac tamponade

A
  • Pericardial effusion that causes hemodynamic compromise
123
Q

Pathophysiology of cardiac tamponade

A
  • Pericardial effusion –> limited diastolic filling
    • –> increased intracardiac pressures and chamber pressure equalization in diastole
    • –> reduced CO
    • results in CARDIOGENIC SHOCK
124
Q

Signs/Symptoms of cardiac tamponade

A
  • Beck’s Triad
    • Hypotension
    • Elevated JVP
    • Quiet heart sounds
  • Pulsus Paradoxus
    • More than a 10 mmHg pressure drop in SBP during inspiration
125
Q

Beck’s Triad

A
  • Hypotension
  • Elevated JVP
  • Quiet heart sounds
  • ***Cardiac Tamponade***
126
Q

Pulsus paradoxus

A
  • More than 10 mmHG pressure drop in SBP during inspiration
  • ***Cardiac Tamponade***
127
Q

What will you see on tests for cardiac tamponade?

A
  • Equalized and elevated diastolic pressures
  • Decreased cardiac output
  • Increased HR (compensatory)
  • RA/RV collapse in diastole
128
Q

Tx for cardiac tamponade

A

pericardiocentesis

129
Q

Constrictive pericarditis causes

A
  • recurrent pericarditis –> calcification of pericardium
  • Radiation
  • Trauma
  • Open heart surgery
130
Q

Signs/symptoms of constrictive pericarditis

A
  • Kussmaul’s sign
    • Distension of jugular veins during inspiration
      • Normally JVP should fall during inspiration
  • Pericardial knock
  • Edema
  • Elevated JVP
  • Ascites
131
Q

Kussmaul’s Sign

A
  • Distension of jugular veins during inspiration
    • Normally JVP should fall
  • **Constrictive pericarditis**
132
Q

Dip and plateau sign

A
  • Constrictive pericarditis
133
Q

Tx for constrictive pericarditis

A
  • pericardiectomy
134
Q

Concentration of oxygen in blood formula

A

CaO2 = (1.34 x O2 Sat x Hb) + (0.003 x PaO2)

135
Q

Alveolar gas equation

A

pAO2 = FiO2 (Patm - PH2O) - (PaCO2/0.8)

136
Q

What does paO2 need to be on 100% O2 in order to say the patient responded to O2?

A

around 600 mmHg

137
Q

What is a normal Aa gradient?

A

(Age/4) + 4

138
Q

Clinical pearl for diffusion block

A

Hypoxic with exertion but not at rest

139
Q

Clinical pearl for hypoventilation

A
  • Usually these people are paralyzed or unconscious
  • Too much morphine or drank till they passed out
140
Q

Widened Aa gradient

A

V/Q mismatch, shunt, diffusion block

141
Q

3 things that cause complete opacification of a hemithorax

A
  1. Massive tumor (usually breast cancer in women)
  2. Very large effusion
  3. Mainstem obstruction –> whole lung collapses
142
Q

Pulm physical exam findings for cancer, effusion, collapsed lung

A
143
Q

Minute Ventilation Formula

A

Minute Ventilation = RR x TV

144
Q

Alveolar Ventilation formula

A

= RR (TV - Dead Space)

145
Q

Cause of low DLCO

A
  • Thickening of alveolar walls - e.g. fibrosis
  • Decreased Surface Area - e.g. emphysema destroys alveolar tissue
146
Q

Low V/normal Q

A

asthma; pneumonia; pulmonary edema. Ventilation is decreased but perfusion is normal.

147
Q

Normal V/low Q (High V/Q ratio)

A

due to increased dead space. It’s seen in pulmonary embolism and emphysema.

148
Q

Hypoventilation clinical pearl

A
  • Aa gradient is normal
    • Clinically people are usually only hypoventilating when they’re unresponsive, like b/c the person is paralyzed on a vent or on too much morphine.
149
Q

diffusion block clinical pearl

A

usually they become hypoxic with exertion but are fine at rest

150
Q

V/Q mismatch and shunt clinical pearls

A
  • Hypoxic at rest
  • Shunt does not correct with O2
151
Q

Compliance Equation

A
152
Q

Plateau Pressure

A

The pressure in your lungs after you inhale and hold it

153
Q

PEEP

A

The pressure in your lungs at the end of exhale

154
Q

Keep plateau pressure below ____ on mechanical ventilation

A

30

155
Q

Keep respiratory rate below ____ on mechanical ventilation

A

35

156
Q

Differential Diagnosis for CXR infiltrate

A
  • Pus = pneumonia
  • Blood = hemorrhage
  • Water = pulmonary edema
  • Gastric juice = aspiration
  • Cells = cancer, fibroblasts
  • Protein = PAP
157
Q

CXR findings correlated to which lung lobe is affected

A
  • Right heart border obscured = right middle lobe
  • Right diaphragm obscured = right lower lobe
  • Mediastinum obscured = right upper lobe
  • Left heart border obscured = lingula
  • Left diaphragm obscured = left lower lung
  • Left mediastinum obscured = left upper lung
158
Q

Reasons for intubation

A
  • Refractory hypoxemia
  • Refractory hypercapnia
  • Decreased mental status/ airway protection
    • Ex: someone is so fucked up their respiratory drive is extremely low
  • Surgery
  • Fatigue/pending respiratory collapse
159
Q

Normal pO2

A

80 mmHg - 100 mmHg

160
Q

Normal pCO2

A

35 - 45 mmHg

161
Q

Acute vs. chronic respiratory acidosis

A
  • Acute = pH decreases by 0.08 for every 10 mmHg change in pCO2
  • Chronic = pH decreases by 0.03 for every 10 mmHg change in pCO2
162
Q

Initial TV for mechanical ventilation

A
  • 6-8 mg/kg (ideal body weight)
163
Q

Initial PEEP for mechanical ventilation

A

5

164
Q

3 Criteria for ARDS

A
  • PaO2/FiO2 ratio less than 300
    • Remember to use decimal for FiO2
  • Bilateral infiltrates
  • Acute onset (less than 14 days)
  • Not cardiac related
165
Q

Complications to avoid with mechanical ventilation

A
  1. Volutrauma
    1. Keep TV at 6 mg/kg
  2. Barotrauma
    1. Keep plateau pressure less than 30
  3. Atelectotrauma
    1. High PEEP (but not so high that plateau pressure goes over 30)
166
Q

How to choose PEEP on ventilator?

A
  • ARDSnet table
  • Keep driving pressure as low as possible, but for sure below 12
    • Driving pressure = plateau pressure - PEEP
167
Q

Differential Dx for cough (wet vs dry, acute vs chronic)

A
168
Q

Differential Dx for bronchiectasis

A
  • CF
  • Chronic infection – e.g. atypical pneumonia (MAC)
  • Immunodeficiencies
  • Rheumatoid Arthritis
  • Inflammatory Bowel Disease
  • Chronic aspiration
169
Q

Tx for CF

A
  1. Airway Clearance – All types of bronchiectasis needs this, not just CF
    1. Hypertonic saline
    2. Percussion/vest
    3. DNAse
    4. Albuterol
    5. Exercise
  2. Antimicrobials
    1. Inhaled antibiotics
    2. Systemic antibiotics
  3. CFTR modulators
    1. Ivacaftor, Lumacaftor, etc
170
Q

Differential Dx for hemoptysis

A
  • Bronchiectasis
  • Trauma
  • Foreign Body
  • Cancer
  • Viral/bacterial pneumonia
  • Pulmonary embolism
  • Pulmonary infarct
  • Septic emboli
  • Mitral stenosis –> causing from a capillary bed leak due to increased pressure
    • All the others are having blood coming from bronchial artery
171
Q

Differential for air bronchograms

A
  • There is fluid in the alveolar sacs = air space disease
  • Pus (pneumonia)
  • Blood
  • Water (pulmonary edema)
  • Cells (organizing pneumonia, cancer)
  • Protein (PAP)
  • Gastric fluid (aspiration)
172
Q

Lung collapse vs. Consolidation physical exam findings

A
173
Q

ARDS pathogenesis

A
  • Alveolar injury
  • Response driven by neutrophils
  • Protein fluid leaks into alveolar space
  • Protein fluid leaks into interstitium –> thickening of interstitium
  • Can damage surfactant and cause lung collapse
174
Q

Causes of ARDS

A
  • Direct lung injury
    • pneumonia
    • aspiration
  • Indirect lung injury
    • sepsis
    • severe trauma with shock
    • acute pancreatitis
175
Q

ARDS diagnosis criteria

A
  • Acute - injury must be within 1 week (or is it 14 days?)
  • Bilateral effusions on CXR
    • Not explainable by cardiac
  • paO2/FiO2 ratio < 300
176
Q

Physiologic derangements in ARDS

A
  • Decreased compliance
    • Due to neutrophilic destruction of surfactant
  • Shunt physiology
    • Fluid in alveolar space –> perfusion but no ventilation
177
Q

Ventilator management strategy for ARDS

A
  • Avoid overinflation
    • Keep Tidal Volume low
    • 6-8 mg/kg of ideal body weight
  • Avoid barotrauma
    • Keep plateau pressure under 30
  • Avoid atelectotrauma
    • Keep PEEP reasonably high
178
Q

Auto PEEP

A
  • Often occurs with people who have obstructive lung diseases and are on a ventilator
  • Not enough time for the expiratory phase –> another breath is given before the person has fully exhaled –> high pressure in the chest
179
Q

What is the problem with Auto PEEP?

A
  • High intrathoracic pressure –> impaired venous return –> low cardiac output
180
Q

Non-ventilator mechanisms to improve oxygenation

A
  • Prone positioning
  • Vasodilators
181
Q

Most important determinant of mortality in ARDS patients

A

Low tidal volume on ventilator

182
Q

How to recognize respiratory failure (and the need for mechanical ventilation)?

A
  • Hypoxemia
    • Low O2 sat even on 100% oxygen
  • Ventilatory (acute) failure
    • pH drops by 0.08 for an increase in pCO2 of 10 mmHg
  • Altered mental status
  • Can’t speak in complete sentences
  • Lots of accessory muscle use
183
Q

invasive vs. non-invasive ventilation

A
  • Invasive = endotracheal tube
  • Non-invasive = Face mask = NPPV
184
Q

Assist Control Setting

A
  • You set TV and respiratory rate
  • They get whatever you set PLUS a full tidal volume any time they try to take a breath on their own
  • Most commonly used ventilator
185
Q

Intermittent Mandatory Ventilation Setting

A
  • You set the TV and respiratory rate
  • They get whatever you set PLUS when they make a breath attempt, they can take in whatever they can generate on their own
    • The machine is not triggered to deliver a full TV the way it is on assist control
  • Considered a weaning mode
186
Q

Pressure Support ventilator setting

A
  • Every time patient makes a breath effort, the machine gives a boost by providing extra pressure
  • Patient must be making respiratory efforts on their own for this to work
  • You do NOT set a RR or TV
187
Q

Sole determinant of plateau pressure

A

lung compliance

188
Q

What determines peak pressure?

A

airway resistance and lung compliance

189
Q

What’s the point of providing end expiratory pressure? (PEEP)

A
  • Prevents atelectasis in alveoli that are at risk of collapsing
190
Q

How to fix AutoPEEP?

A
  • Actually increase TV and decrease respiratory rate
  • Gives patient more time to exhale –> less breath stacking
191
Q

How to manage high pressures as a complication of mechanical ventilation?

A
  1. If high peak pressure but normal plateau –> due to airway resistance –> suction, bronchodilators
  2. If high peak and plateau pressures –> due to lung compliance (you’re on the upper part of the curve) –> decrease tidal volume
192
Q

How to recognize and fix overventilation (mechanical ventilation complication)?

A
  • Patient is making no spontaneous breathing attempts on A/C mode
  • Can see respiratory alkalosis
  • Reduce TV or RR
193
Q

Why is high FiO2 problematic?

A
  • Hyperoxia can damage lungs due to reactive oxygen species
  • We try to get them off 100% oxygen
194
Q

Dysynchrony

A
  • Patient is trying to exhale when ventilator is delivering another breath
  • Causes anxiety and discomfort
  • Fix w/ increased sedation or changing ventilator mode
195
Q

How to prevent pneumonia on mechanical ventilation?

A
  • Try to keep head elevated 30 - 45 degrees
  • Suction frequently
196
Q

Rapid shallow breathing index

A
  • RR/TV
  • Used to determine when someone is ready to come off ventilator
  • Lower number = better predictor of success
    • i.e. low RR and high TV
197
Q

CPAP

A
  • CPAP = continuous positive airway pressure
    *
198
Q

BIPAP

A
  • similar to pressure support where each inspiration is supported by a set pressure. An expiratory pressure is also set
199
Q

Interstitial Lung Disease definition

A
  • Cells in the interstitium (NOT alveolar space) that shouldn’t be there and they are NOT due to cancer or infection
200
Q

Interstitial Lung Disease pathophysiology

A
  • Fibrosis of interstitium
    • Decreased lung compliance
    • Decreased DLCO
    • Widened A-a gradient
201
Q

Most common interstitial lung diseases

A
  • Idiopathic pulmonary fibrosis
  • Chronic hypersensitivity pneumonitis
  • Sarcoidosis
  • Connective Tissue Disorder - ILD
202
Q

Symptoms of ILD

A
  • SOB that progresses over time
    • Often contributed to “being out of shape”
  • Dry cough
  • Can have other symptoms depending on the specific disease
    • ex: CTD-ILD you see autoimmune related changes like skin issues and joint pain
203
Q

CTD-ILD vs. idiopathic pulmonary fibrosis

A
  • IPF more common in older adults (50s/60s) vs. CTD-ILD is more common in younger adults (30s/40s)
  • IPF is more common in males vs. CTD-ILD is more common in females
204
Q

Signs of interstitial lung disease

A
  • Crackles during physical exam are possible
  • Impaired DLCO
  • Restrictive Lung Disease PFT’s
    • Normal/High FEV1/FVC ratio
    • Low FEV1 and FVC overall
205
Q

UIP pattern

A
  • Honeycombing
  • Traction bronchiectasis
206
Q

Most common diagnosis with UIP pattern

A

Idiopathic pulmonary fibrosis

207
Q

How do we make a diagnosis of idiopathic pulmonary fibrosis?

A
  • It’s a diagnosis of exclusion
  • Rule out autoimmune issues (by ordering labs/panels) – rules out CTD-ILD
  • Rule out exposure-related – hypersensitivity pneumonitis, asbestos
  • Rule out drug exposure causes
208
Q

What is the NSIP pattern?

A
  • Ground glass on CT
  • Traction bronchiectasis
209
Q

CTD-ILD presentation

A
  • autoimmune issues - raynaud’s, stiff joints, thickening of skin on arms
  • Dry, chronic cough
  • shortness of breath
  • May present with UIP or NSIP pattenr
210
Q

Sarcoidosis features

A
  • Upper lung predominant
  • non-necrotizing granulomatous inflammation
  • Bilateral hylar lymphadenopathy
    • See on CXR or CT
211
Q

Differential diagnosis of a patient presenting with interstitial lung disease

A
  • Exposure-related?
    • Hypersensitivity pneumonitis
    • Pneumoconiosis
  • Autoimmune related?
    • CTD-ILD
  • Sarcoidosis
    • Enlarged lymph nodes
  • UIP pattern?
    • Often IPF
  • NSIP pattern
    • Can be lots of things
212
Q

Exposure-related interstitial lung diseases

A
  • Hypersensitivity pneumonitis
    • Bird proteins
    • Mold
  • Pneumoconiosis
    • Coal
    • Quartz
    • Asbestos
213
Q

Hypersensitivity pneumonitis is usally upper lung/lower lung predominant?

A

upper lung

214
Q

IPF is usually upper lung/lower lung predominant?

A

lower lung

215
Q

Normal paO2

A

80 - 100 mmHg

216
Q

Normal paCO2

A

35 - 45 mmHg

217
Q

apnyc threshold

A
  • When you decrease paCO2 enough, either through hyperventilation or mechanical ventilation, you will eventually drop your respiratory drive to 0.
  • This point where respiratory drive is 0 = apnyc threshold
218
Q

Arterial blood gas notation

A
  • pH/pCO2/pO2/HCO3-
  • ex: 7.4/40/90/24
219
Q

Normal bicarb levels

A

23 - 30

220
Q

Normal pH

A

7.35 - 7.45

221
Q

pH changes with chronic respiratory acidosis

A
  • pH decreases by 0.03 for every 10 mmHg increase in pCO2
222
Q

pH changes with acute respiratory acidosis

A

pH decreases by 0.08 for every 10 mmHg increase in pCO2

VF1 - Block 3 (7 decks)

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