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PT 5 Flashcards

1
Q

What are the 3 processes involved in gas exchange

A
  1. Ventilation
  2. Perfusion
  3. Diffusion
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2
Q

What is ventilation

A

Moving gases into and out of the lungs

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3
Q

What is perfusion

A

Cardiovascular system sending oxygenated blood to tissue and returning de-oxygenated blood back to the lungs

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4
Q

What is diffusion

A

Moving respiratory gases from one area to another by concentration gradient

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5
Q

What is included in the upper respiratory tract

A

Nose, mouth, pharynx, epiglottis, larynx and trachea

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6
Q

What is included in the lower respiratory tract

A

Bronchi, bronchioles, alveolar ducts and lung lobes

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7
Q

What lung is more likely to have aspiration due to having a shorter bronchous

A

Right lung

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8
Q

How many lobes are in the right and left

A

Right has three

Left has two

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9
Q

Who is at risk of atelectasis

A
  • Post op patients due to anesthesia and restrictive breathing
  • Acute respiratory distress syndrome (no surfactant)
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10
Q

What is PaO2

A

Partial pressure of oxygen in arterial blood (amount of oxygen dissolved in plasma)

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11
Q

What is SaO2

A

Arterial oxygen saturation (amount of oxygen bound to hemoglobin)

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12
Q

What is compliance of the lungs

A

How easily the lungs expand - when compliance is decreased, it makes it difficult for the lungs to inflate (like in COPD)

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13
Q

What is elastic recoil

A

The tendency for the lungs to return back to their original size

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14
Q

What is resistance

A

Any impediment to airflow during inspiration or expiration

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15
Q

What are the two types of lower respiratory tract problems

A
  • Restrictive: chest wall and diaphragm can’t fully expand

- Obstructive: Resistance of airflow due to airway obstruction or narrowing

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16
Q

What are examples of extra-pulmonary restrictive disorders (outside of the lungs)

A
  • Head injuries
  • Spinal cord injuries
  • Muscular dystrophy
  • Chest wall trauma
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17
Q

What are examples of intra-pulmonary restrictive disorders

A
  • Pleural effusion
  • Pleurisy
  • Pneumothorax
  • Acute respiratory distress syndrome (ARDS
  • Atelectasis
  • Interstitial lung diseases
  • Pneumonia
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18
Q

What are examples of obstructive pulmonary disorders

A
  • Asthma
  • Emphysema
  • COPD
  • Cystic fibrosis
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19
Q

What are disorders of the upper respiratory system

A
  • Epistaxis (nosebleeds)
  • Allergic rhinitis (inflammation of the nasal mucosa due to an allergen)
  • Acute viral rhinitis
  • Influenza
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20
Q

What can prolong a nosebleed (epistaxis)

A

Taking aspirin, NSAIDs, warfarin or other anticoagulant drugs

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21
Q

How do you care for a nosebleed

A
  1. Have pt sit down, with head titled slightly forward
  2. Apply direct pressure by squeezing the nostrils together for 5-15 minutes
  3. Seek medical assistance if bleeding doesn’t stop in 15 minutes
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22
Q

What can be used to treat posterior nosebleeds

A

Epistaxis balloons (inflates in the back of the nose to apply pressure, to help stop the bleed)

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23
Q

What is pneumonia infecting

A

The lung parenchyma (gas exchange portion of the lungs)

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24
Q

How do we get pneumonia

A

When pathogens reach the lungs and defense mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents

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25
Q

How can pathogens get into the lungs and cause pneumonia (examples - not an exhaustive list) 7

A
  • Weak cough or epiglottal reflex may allow aspiration to get into the lungs
  • Tracheal intubation, which bypasses normal filtration processes and interferes with the cough reflex and mucociliary escalator mechanism
  • Mucociliary mechanism is impaired (self-cleaning mechanism of the airway)
  • Air pollution
  • Smoking
  • Aging 65+
  • Bed rest, prolonged immobility
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26
Q

What are three ways that organisms reach the lungs and cause pneumonia

A
  1. Aspiration from nasopharynx or oropharynx (normal organisms that cause pneumonia live in our mouth and throat)
  2. Inhalation of microbes present in air (mycoplasma pneumonia and fungal pneumonia)
  3. Hematogenous spread from a primary infection elsewhere in the body (spread by bloodstream) (example strep or staph from endocarditis)
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27
Q

Describe the pathophysiology of pneumonia 4

A
  1. Inflammatory response - bringing neutrophils to fight and kill off the pathogens, this causes edema, which then causes fluid to leak from the capillaries and tissues into the alveoli
  2. This fluid leak, causes the alveoli to fill with fluid and debris (consolidation - when fluid fills a part of your lungs that is normally filled by air)
  3. You also have an increase in mucus production, which leads to airway obstruction
  4. Both consolidation and airway obstruction lead to a decrease in O2 transportation, resulting in hypoxia
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28
Q

What types of things can cause pneumonia 6

A
  • Bacteria
  • Viruses
  • Mycoplasma
  • Fungi
  • Parasites
  • Chemicals
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29
Q

What are the three ways to classify pneumonia

A
  1. Community acquired pneumonia (CAP)
  2. Hospital acquired pneumonia (HAP)
  3. Ventilator associated pneumonia (VAP)
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30
Q

Why is it important to know what class of pneumonia it is

A

Once we know what is causing it, then we can treat it

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31
Q

What is community acquired pneumonia

A

Occurs in pts who have not been hospitalized or have lived in a long-term care facility within 14 days of the onset of symptoms

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32
Q

What are the most common organisms causing CAP

A
  • Legionella pneumophila
  • MRSA
  • s. pneumoniae
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33
Q

What are the most common organisms causing HAP 4

A
  • Acinetobacter species
  • E. coli
  • Klebsiella pneumoniae
  • Pseudomons aeruginosa
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34
Q

If someone has pneumonia, what scoring system can we use to determine if the pt is high risk for death and should be hospitalized

A

CURB-65

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35
Q

What are the 8 factors of CURB

A 
C: are they confused?
U: Is their BUN greater than 20?
R: Is their respiratory rate at or greater than 30?
B: Is their BP less than 90/60?
- Are they at 65 or older?
- Is their LDH above 230?
- Is their albumin less than 3.5?
- Is their platelet count less than 100?
(If yes, each counts for 1 point)
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36
Q

What are the points for pneumonia based on CURB

A
  • 0-2 = outpatient
  • 3-4 = In patient
  • 5-8 = ICU
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37
Q

Once pneumonia is suspected, what should happen

A

The pt should go on empiric antibiotic therapy asap, even without knowing the causative agent - basically you’re giving them an antibiotic based on the diagnosis of CAP, HAP, VAP, risk factors, early versus late onset, presentation, underlying medical conditions, hemodynamic stability, likely causative pathogen. The antibiotic can be adjusted once sputum cultures come back.

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38
Q

What is hospital acquired pneumonia (HAP)

A

pneumonia in a non-intubated pt that begins 48 hrs or longer after admission to the hospital, and was not present at the time of admission

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39
Q

What is ventilator associated pneumonia (VAP)

A

pneumonia that occurs 48hrs after endotracheal intubation

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40
Q

Are they always going to do a sputum culture for someone that is not high risk and going in as outpatient

A

No, probably not. They’re most likely going to give you antibiotics and send you on your way. They’ll probably get a sputum culture if you have HAP or VAP.

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41
Q

What is a major issue with pneumonia

A

Multi-drug resistant (MDR) organisms (staphylococcus aureus, gram-negative bacilli, MRSA)

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42
Q

What are risk factors for MDR pneumonia 4

A
  • Advanced age
  • Immunosuppresion
  • History of abx use
  • Prolonged mechanical ventilation
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43
Q

What is aspiration pneumonia

A

When something abnormal enters your trachea and lungs from your mouth or stomach

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44
Q

What are risk factors for aspiration pneumonia 3

A
  • Decreased level of consciousness
  • Difficulty swallowing
  • NG tubes
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45
Q

What types of aspirated material can cause aspiration pneumonia 4

A
  • Food
  • Water
  • Vomitus
  • Secretions
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46
Q

What is the most common type of infection in aspiration pneumonia

A

Bacterial infection

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47
Q

What if aspiration pneumonia is caused by acidic gastric contents?

A

This causes chemical (noninfectious) pneumonitis, and may not need antibiotics.

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48
Q

What is necrotizing pneumonia

A

From a bacterial lung infection, usually from CAP, where the lung tissue turns into a thick, liquid mass.

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49
Q

What are the signs and symptoms of necrotizing pneumonia

A
  • Immediate respiratory insufficiency and/or failure
  • Leukopenia (Low WBCs)
  • Bleeding into the airways
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50
Q

What is opportunistic pneumonia

A

Inflammation and infection of the lower respiratory tract in immunocompromised patients

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51
Q

What patients are at risk for opportunistic pneumonia 4

A
  • Severe protein-calorie malnutrition
  • Immunodeficiencies (HIV)
  • Chemo/radiation pts.
  • Long-term corticosteroid pts
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52
Q

What is pneumocytis jiroveci pneumonia (PJP)

A

pneumonia that is most common in people with HIV. It causes diffuse bilateral infiltrates and consolidation of the lungs, which can lead to acute respiratory failure and death. It can also spread to other organs like the liver, bone marrow, lymph nodes, spleen and thyroid.

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53
Q

What do we treat PJP with

A

Trimethoprim/sulfamethoxazole IV or orally

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54
Q

What causes cytomegalovirus (CMV)

A

Herpesvirus

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55
Q

Most CMV is asymptomatic or mild, however, it can cause severe disease in whom

A

People with an impaired immune response (ie transplant pts, chemo pts)

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56
Q

How can we treat CMV

A

Antiviral medications and high-dose immunoglobulin (antibodies)

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57
Q

What are complications of packing a nosebleed

A

They can be painful (give pain medicine) and they can put the pt at risk for infection from bacteria (might give antibiotics)

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58
Q

What are the most common clinical manifestations of pneumonia 7

A
  1. Cough
  2. Fever
  3. Chills
  4. Dyspnea
  5. Tachypnea
  6. Pleuritic chest pain
  7. Green, yellow or rust colored sputum
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59
Q

What are some nonspecific manifestations of pneumonia 5

A
  • Diaphoresis
  • Anorexia
  • Fatigue
  • Myalgias (muscle aches and pain)
  • Headache
    (pneumonia symptoms are not just about respiratory)
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60
Q

Older adults and debilitated pts don’t usually have the typical symptoms of pneumonia… What do they usually have 2

A
  • Confusion or stupor

- Hypothermia instead of a fever

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61
Q

What might viral pneumonia start as

A

Influenza, which then can lead to viral pneumonia

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62
Q

When examining someone with pneumonia, what might you find 5

A
  • Fine or coarse crackles
    If they have consolidation:
  • Bronchial breath sounds
  • Egophony (change in sound of voice)
  • Increased fremitus (vibration of chest wall from vocalization)
  • Dullness to percussion if pleural effusion is present
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63
Q

What are other complications from pneumonia 10

A
  • Atelectasis (collapsed airless, aveoli)
  • Pleurisy (inflammation of the pleura)
  • Pleural effusion (fluid in the pleural space, usually the fluid is sterile and is absorbed in 1-2 weeks, might need thoracentesis)
  • Bacteremia (bacterial infection in the blood)
  • Pneumothorax (air collets in the pleural space, causing the lung to collapse)
  • Meningitis
  • Acute respiratory failure (can’t exchange O2 and Co2 anymore - leading cause of death from severe pneumonia)
  • Sepsis/septic shock (Bacteria from alveoli enter the bloodstream)
  • Lung abscess (not common)
  • Empyema (rare, accumulation of purulent exudate in the pleural cavity - requires abx and chest tube)
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64
Q

What usually gives us enough information to diagnosis pneumonia 3

A
  • History
  • Exam
  • Chest x-ray
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65
Q

Do we always get a sputum culture and gram stain for pneumonia

A

Usually not for CAP. You also shouldn’t delay treatment by waiting for these test, as this can increase morbidity and mortality.

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66
Q

With bacterial pneumonia, what diagnostic finding can be seen

A

Leukocytosis, where there is an increase in the WBC above 15,000. You also have bands (immature neutrophils)

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67
Q

When looking at ABGs with pneumonia, what might we find

A
  • Hypoxemia when PaO2 is less than 80
  • Hypercapnia when PaCO2 is greater than 45
  • Acidosis when pH is less than 7.35
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68
Q

What is the normal range of PaO2

A

80-100

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69
Q

What is the normal range of SaO2

A

> 95%

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70
Q

What is the normal range of PaCO2

A

35-45

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71
Q

What is the normal range of HCO3

A

22-26

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72
Q

What are some other diagnostic studies you might do for pneumonia (besides the main ones)

A
  • Blood cultures for the seriously ill
  • Thoracentesis and/or bronchoscopy with washings to obtain fluid samples when pts aren’t responding to initial therapy
  • Looking at biologic markers like C-reactive protein (CRP), kallistatin and procalcitonin
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73
Q

What can be given to prevent streptococcus pneumoniae

A

The pneumococcal vaccine

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74
Q

Who should get the pneumococcal vaccine

A
  • Children younger than 2
  • Adults 65 and older
  • Or those between 2-65 who are high risk
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75
Q

When should the pt respond to abx tx for pneumonia. What will we see?

A

Within 48-72hrs. Decreased temp, improved breathing, reduced chest discomfort.

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76
Q

When would we repeat a chest x-ray after pneumonia tx

A

6-8 weeks

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77
Q

Besides given abx, what else can be given to help support a pt with pneumonia 4

A
  • Oxygen for hypoxemia
  • Analgesics for chest pain
  • Antipyretics
  • Tailor rest and activity
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78
Q

Are cough suppressants, mucolytics, bronchodilators, and corticosteroids prescribed as adjunctives for pneumonia

A

Yes - but there probably only useful if someone has an underlying chronic condition and needs them

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79
Q

If someone has pneumonia , do we want them to get more or less movement

A

More movement, to help mobilize those secretions

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80
Q

Is there a tx for viral pneumonia

A

Not really, usually care is supportive, and it should resolve in 3-4 days.

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81
Q

Once you classify pneumonia (CAP, HAP, VAP), what drug therapy do you use

A

Empiric therapy - where you are basing the drug therapy on the likely pathogen and risk factors for MDR

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82
Q

When should you see drug therapy improvement of pneumonia

A

3-5 days

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83
Q

Do you start with an IV or oral meds first for pneumonia

A

Usually start with IV meds, and then switch to oral as soon as the pt is stable.

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84
Q

How long is CAP tx? When is it stopped?

A

Lasts a minimum of 5 days. Pt should be afebrile (not feverish) for 48-72 hrs before tx can be stopped.

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85
Q

Why is hydration important for pneumonia

A

It helps thins and loosens secretions

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86
Q

Should people with pneumonia have big meals or small meals?

A

Small, frequent meals due to dyspnea. Want them high in calories.

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87
Q

What are some questions you may want to ask a pt when you suspect pneumonia 6

A
  • Past health history
  • Use of abx, corticosteroids, chemo or immunosuppressants
  • Recent surgeries
  • Recent intubation
  • Tube feedings
  • Pain (ie with breathing)
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88
Q

What is some objective data you may gather if you suspect pneumonia 13

A
  • Fever
  • Restlessness or lethargy
  • Splinting affected area
  • Tachypnea
  • Asymmetric chest movements
  • Use of accessory muscles
  • Crackles
  • Friction rub
  • Dullness on percussion
  • Increased tactile fremitus
  • Sputum amount and color
  • Tachycardia
  • Changes in mental status
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89
Q

What can help reduce VAP

A

Adhering to all aspects of the ventilator bundle

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90
Q

How can we help prevent pneumonia in at risk pts 6

A
  • Keep HOB elevated at or above 30 degrees
  • Assist with eating, drinking and taking meds
  • Assess for gag reflex before giving food or fluids
  • Early mobilization
  • IS
  • Twice-daily oral hygiene with chlorhexidine swabs for post-op pts.
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91
Q

What would be a concerning finding when assessing a pt diagnosed with influenza:
a - sore throat, and headache
b - cough, with chest discomfort
c - crackles, with diminished breath sounds
d - fever of 102

A

C = indicates pneumonia (pneumonia is a complication of influenza)

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92
Q

What are complications of influenza 4

A
  • Bronchitis
  • Pneumonia
  • Acute respiratory failure
  • ARDS (acute respiratory distress syndrome)
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93
Q

What can cause nosebleeds 12

A
  • Trauma
  • Hypertension
  • Low humidity
  • Upper respiratory tract infections
  • Allergies
  • Sinusitis
  • Foreign bodies
  • chemical irritants (street drugs)
  • Overuse of decongestant nasal sprays
  • Facial or nasal surgery
  • Anatomic malformation
  • Tumors
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94
Q

Which is more difficult to treat, anterior or posterior nosebleeds

A

Posterior

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95
Q

Who often has posterior nosebleeds

A

Older adults with other problems like hypertension (hard to determine how much blood is lost because they are so close to the throat)

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96
Q

How can you treat an anterior nose bleeds

A
  • Use a pledget (nasal tampon) with lidocaine
  • Vasoconstrictive agents like epinephrine placed in the nose
  • Keep packed for 48-72 hrs
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97
Q

TB most commonly infects the lungs, but what else can it infect

A
  • Brain
  • Kidneys
  • Bones
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98
Q

What is the leading cause of death in patients with HIV/AIDs

A

TB

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99
Q

When is a strain of TB classified as multidrug-resistant TB

A

When it is resistant to the first-line antitubercular drugs (isoniazid and rifampin)

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100
Q

When is a strain of TB classified as extensively drug-resistant TB

A

When the strain is also resistant to the first-line drugs and any fluoroquinolones plus injectable antibiotics

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101
Q

What can cause TB to become resistant 3

A
  • Incorrect prescribing
  • Lack of case management
  • Nonadherence
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102
Q

How is TB spread

A

Through airborne particles

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103
Q

How long can TB particles hang in the air

A

Minutes to hours

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104
Q

How do the TB particles get into the air

A

Through breathing, talking, singing, sneezing or coughing

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105
Q

Can you get TB by touching, sharing food utensils, kissing or other types of physical contact

A

No

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106
Q

Once you inhale TB, where do the particles go

A

Into your bronchioles and alveoli

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107
Q

Once TB is inhaled, what happens in the body

A

An inflammatory response occurs - calcified TB granuloma is created called a Ghon lesion or focus - this granuloma walls off the infection and prevents further spread - about 90% of the time TB does not develop due to this immune response

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108
Q

If you body is unable to fight off TB, when would we see it start to multiply

A

Months - years later

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109
Q

Even though TB is aerophilic (oxygen loving) and has an affinity for the lungs, what can it do

A

It can spread to other organs and grow as well

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110
Q

What are the 3 classifications of TB

A
  • Primary infection
  • Latent TB infection
  • Active TB disease
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111
Q

What is primary infection of TB

A

When TB is inhaled and your immune response can’t stop the spread.

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112
Q

What is a latent TB infection

A

They have TB, but it is not active.

  • Asymptomatic
  • Can’t transmit TB, but can develop TB at some point.
  • Immunosuppression, diabetes, poor nutrition, aging, pregnancy, stress and chronic disease can reactivate the TB
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113
Q

What is active TB disease

A

Could have primary TB or reactivation TB

  • Primary TB: when active TB develops within the first 2 years of infection (HIV pts at greatest risk of this TB)
  • Reactivation TB (post-primary): when TB develops after 2 years of the infection
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114
Q

When would you see symptoms of pulmonary TB (active)

A

Usually in 2-3 weeks

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115
Q

What are pulmonary TB symptoms 3

A
  • Initial dry cough that becomes productive and frequent
  • Constitutional symptoms (fatigue, malaise, anorexia, weight loss, low-grade fever, night sweats)
  • Dyspnea and hemoptysis (spitting of the blood) are late symptoms (not common)
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116
Q

TB can also present more acutely, what are some of those symptoms 5

A
  • High fever
  • Chills (flu like symptoms)
  • Pleuritic pain
  • Productive cough
  • Crackles and/or adventitious breath sounds
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117
Q

What are extrapulmonary symptoms of TB

A

Depend on the organs infected
Examples:
- Renal TB can cause dysuria and hematuria
- Bone TB can cause severe pain
- Meningitis TB can cause headaches, vomiting, and lymphadenopathy

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118
Q

How are TB symptoms diff. for immunosuppressed and older adult pts

A

They are less likely to have a fever and show other signs of infection

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119
Q

What is the issue with HIV and TB symptoms

A

Symptoms of TB in HIV pts can look like other opportunistic infections (like PJP - pneumonia in immunocompromised pts). Need to carefully investigate the cause.

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120
Q

What may be the only symptom of TB in older adults

A

Change in cognitive function

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121
Q

Once pulmonary TB is treated, will there be any complications

A

No, there are not usually any complications if properly treated. There may be some scarring and residual cavitation within the lungs. Significant damage can occur in pts who are poorly treated or who do not respond to tx.

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122
Q

What is miliary TB

A

A complication of TB that has spread through the bloodstream to other organs

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123
Q

What are symptoms of miliary TB 5

A
  • Fever
  • Cough
  • Lymphadenopathy (swelling of lymph nodes)
  • Hematomegaly (enlarged liver)
  • Splenomegaly (enlarged spleen)
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124
Q

What is pleural TB

A

A complication of TB where bacteria get into the pleural space, which triggers an inflammatory response and a pleural exudate of protein-rich fluid (called unilateral pleural effusion)

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125
Q

What are symptoms of pleural TB 4

A
  • Chest pain
  • Fever
  • Cough
  • Empyema (large number of TB organisms in the pleural space - less common)
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126
Q

What type of pneumonia can TB cause

A

Bacterial pneumonia

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127
Q

What can happen if TB gets into the spine

A

It can cause Pott’s disease, which leads to the destruction of the intervertebral disc and adjacent vertebrae

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128
Q

What can happen if TB gets into the CNS

A

Bacterial meningitis

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129
Q

What can happen if TB gets into the abdomen

A

Peritonitis (inflammation of the peritoneum which lines the abdomen) (commonly seen in HIV positive patients)

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130
Q

Explain the TB skin test (mantoux test)

A
  • Inject purified protein derivate (PDD) intradermally
  • Assess for induration in 48-72 hrs
  • Presence of induration (not redness) at the injection site indicates development of antibodies to TB exposure
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131
Q

What does induration look like

A

Palpable, raised, hardened area or swelling (no redness)

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132
Q

When would antibodies form after TB exposure

A

2-12 weeks

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133
Q

How big should the induration be if a low-risk individual has TB

A

15mm or bigger

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134
Q

How big should the induration be if a immunocompromised pt is positive for TB

A

5mm or bigger

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135
Q

What are the interferon-y gamma release assays (IGRAs)? What do they test for? What are the advantages and disadvantages?

A

The quantiferon-TB and T-SPOT.TB tests.

  • They detect T-cells in response to mycobacterium tuberculosis
  • They provide rapid results, require only one visit, no reader bias, no booster phenomenon not affected by bacilus calmette-guerin (BCG) vaccine
  • Downside = expensive
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136
Q

What is the deal with this BCG vaccine?

A

Vaccine for TB given in other countries, where there is a high risk of TB. Can make the skin test look positive, but not the IGRAs.

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137
Q

Can you make a diagnosis of TB solely on a chest x-ray? Why or why not?

A

No you can’t, because some pts may have a normal chest x-ray even though they have TB

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138
Q

What would a chest x-ray look like to suggest someone may have TB

A
  • Upper lob infiltrates
  • Cavity infiltrates
  • Lymph node involvement
  • Pleural and/or pericardial effusion
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139
Q

What is the gold standard for diagnosing TB

A

Sputum culture

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140
Q

Explain TB sputum culture tests. What’s the downfall?

A

Have to give 3 consecutive sputum cultures, with 8-24 hr intervals. Results can take up to 6 weeks.
Downfall- you may have pts that are not compliant and do not come back for their consecutive tests.

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141
Q

Are most people hospitalized with TB

A

No, most people are treated on an outpatient basis

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142
Q

What should a pt do if they have a positive sputum smear test

A

They are considered infectious for the first 2 weeks after starting treatment. Basically they need to quarantine.

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143
Q

What should I really remember about TB

A

It’s really difficult to get people to comply with tx, because the tx can be pretty brutal.

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144
Q

What is tx like for active TB

A

Aggressive.
Two phases:
- Initial lasting 8 weeks
- Continuation lasting 18 weeks

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145
Q

What are the 4 drugs used for active TB

A
  • Isoniazid
  • Rifampin
  • Pyrazinamide
  • Ethambutol
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146
Q

What do we worry about with the active TB drugs, especially isoniazid

A

They can cause hepatotoxicity and nonviral hepatitis

  • Monitor liver function every 2-4 weeks
  • Avoid alcohol
  • Watch for signs of hepatitis at the start and during tx.
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147
Q

What if someone has a reaction to the 4 drugs for active TB treatment

A

There are alternatives like rifabutin and rifapentine.

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148
Q

What will help guide us when developing tx for MDR-TB

A

Using sensitivity testing

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149
Q

Describe directly observed therapy (DOT) for TB

A

Giving TB drugs directly to the pts and watching them swallow the pills.

  • Preferred strategy for all TB patients, especially those at risk for non-compliance
  • Nonadherence is a major factor in the emergence of MDR-TB
  • Public health nurses administer at clinic sites
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150
Q

What do we give to treat latent TB and for how long (helps prevent latent from forming into active)

A

Isoniazid for 6-9 months

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151
Q

How long should HIV pts with latent TB take isoniazid for

A

9 months

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152
Q

What if a person is pretty much healthy and they have latent TB, what could the tx look like for them

A

If they don’t do the standard, then they can do a 3 month regimen of isoniazid and rifapentine. Or 4 months of rifampin if allergic to isoniazid.

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153
Q

When doing our physical assessment for someone with suspected TB, what are we doing/look for

A
  • Productive cough
  • Night sweats
  • Afternoon temp elevation
  • Wt loss
  • Pleuritic chest pain
  • Crackles over apices of lungs
  • Sputum collection
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154
Q

What do we do if someone has TB in the hospital 5

A
  • Put them in a room by themselves with 6-12
  • Negative pressure room (traps air inside to protect those outside)
  • Wear high-efficiency particulate air (HEPA) masks
  • Have pt wear mask outside of room to protect others
  • Identify and screen close contacts.
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155
Q

What TB drug can turn your urine red-orange

A

Rifampin

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156
Q

What are some basic things you want to teach someone with TB 2

A
  • Cover mouth when coughing

- Wash hands

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157
Q

What type of disease is asthma

A

An obstructive pulmonary disease

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158
Q

What are risk factors for asthma 5

A
  • Genetics
  • Environment (pollen, pollutants)
  • Being a male as a child (no risk as an adult)
  • Obesity
  • Smoking
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159
Q

What is interesting about allergens and asthma

A

They may not actually cause someone to have asthma, but they can trigger asthma symptoms

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160
Q

What are types of allergen triggers for asthma 5

A
  • Cockroaches
  • Furry animals
  • Fungi
  • Pollen
  • Molds
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161
Q

When might exercise-induced asthma or bronchospasms trigger asthma

A
  • After vigorous exercise

- After exposure to cold air

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162
Q

What do we worry about with stagnant air and asthma

A

The stagnant air can lead to concentrated pollution in the atmosphere and trigger asthma

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163
Q

What is the most common job-related respiratory disorder

A

Asthma (working around chemicals for your job can trigger asthma)

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164
Q

What’s the issue with asthma and respiratory infections

A

These infections can trigger acute asthma attacks

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165
Q

What are other common triggers of asthma 5

A
  • Nose and sinus problems
  • Medications
  • Food additives and allergies
  • GERD
  • Emotional stress (cause hyperventilation and hypocapnia = narrow airway)
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166
Q

What medications can trigger asthma attacks and why 3

A
  • Aspirin and NSAIDs (pts are sensitive to these drugs, so they can trigger an attack)
  • Beta blockers can cause bronchospasm (blocks HR and lungs)
  • ACE inhibitors can cause a dry, hacking couch which can make asthma symptoms worse
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167
Q

How can GERD trigger asthma

A

It can cause bronchoconstriction and aspiration. And asthma drugs may worsen GERD symptoms.

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168
Q

Basically, what is the pathophys of asthma

A

There’s a trigger, which causes your immune system to respond, which then causes bronchoconstriction, hyperresponsiveness (hyperreactivity), edema of airways, congestion, thick mucus, bronchial muscle spasms, thickening of airway walls (these are usually what we see in early-phase).

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169
Q

When does the early-phase response occur with asthma

A

Within 30-60 minutes after exposure

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170
Q

When does the late-phase response occur

A

4-6hrs after initial attack

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171
Q

What’s happening in late-phase asthma 4

A
  • Can be more severe than early
  • Can last for 24hrs or more
  • Not treated or resolved, can lead to irreversible lung damage
  • Structural changes in bronchial wall called remodeling occur
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172
Q

What are the clinical manifestations of asthma

A
  • Wheezing
  • Breathlessness
  • Cough
  • Tight chest
    (may be abrupt or gradual)
    (may last from minutes-hrs)
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173
Q

What is interesting about asthma symptoms

A

Expiration can be longer than inspiration since there is bronchospasm, edema and mucus, it takes longer to move the air out of the lungs

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174
Q

What is the only symptom of cough variant asthma

A

A cough because the bronchospasm is not severe enough to cause airflow obstruction

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175
Q

What are the 4 classifications of asthma

A
  • Intermittent
  • Mild persistent
  • Moderate persistent
  • Severe persistent
176
Q

What are the severe exacerbations of asthma 6

A
  • RR above 30
  • Dyspnea at rest, feeling suffocated
  • Pulse greater than 120
  • PERF 40% at best (peak expiratory flow rate - measured by the peak flow meter to test lung function)
  • Accessory muscles in neck with be bulging
  • Can be combative and confused due to low sats
177
Q

What the life-threatening exacerbations of asthma

A
  • Too dyspneic to speak
  • Perspiring profusely
  • Drowsy/confused
  • PERF below 25%
178
Q

What can you use to help diagnosis asthma 7

A
  • History and physical
  • Spirometry
  • Peak expiratory flow rate using a peak flow meter
  • Chest x-ray (will look normal if pt is asymptomatic)
  • Oximetry
  • Allergy testing
  • Elevated levels of eosinophils and IgE (these suggest that there may be a genetic risk factor for developing asthma)
179
Q

What tool do HCP base drug therapy on for asthma pts

A

They use a step approach. If the patient is doing well, then they can step down the medication, if they are doing worse, then they can step up the medications

180
Q

What are the two types of asthma drugs

A
  • Short-term rescue/reliever medication

- Long-term or controller medication

181
Q

What is the “rescue” medication of asthma

A

B2-adrenergic agonist (SABA) = albuterol

182
Q

What are the long term medications for asthma

A

Your inhaled corticosteroids (ICS) like fluticasone. Might also be used with long-acting bronchodilators (LABS)

183
Q

How should someone take albuterol in a rescue situation

A

Take 2-4 puffs every 20 minutes. Repeat three times.

184
Q

What am I checking for during an assessment for asthma 8

A
  • Look at RR
  • HR
  • Are they using accessory muscles
  • Do I hear wheezing (in an asthmatic, I am more concerned when I don’t hear wheezing)
  • Percussion of lungs
  • PERF (difficult to get during an acute asthma attack)
  • ABGs
  • Pulse ox
185
Q

What do the ABGs look like for asthmatics at first

A

At first, they are hyperventilating from the hypoxemia, so we will see a decrease in PaCO2 and an increase in pH

186
Q

What PERF number shows an obstruction

A

Less than 200 L/min

187
Q

What is one thing you don’t want to hear in an asthmatic pt

A

A “silent chest”

188
Q

What does a “silent chest” look like and indicate

A

There will be diminished breath sounds, no wheezing, pt will be struggling. This is a life-threatening situation - going into respiratory failure

189
Q

When someone is having a severe asthma attack, what are we carefully monitoring 3

A
  • HR
  • RR and rhythm
  • BP
190
Q

How are we treating someone with severe and life-threatening asthma exacerbations

A
  • IV magnesium sulfate (bronchodilator)
  • 100% oxygen
  • Hourly or continuous nebulized SABA
  • IV corticosteroids
191
Q

What medication is the fast acting drug for asthma

A
  • albuterol (it’s a short acting beta 2 agonists (SABA) bronchodilator)
192
Q

What types of anti-inflammatory drugs may be prescribed for long-term asthma control

A
  • Inhaled corticosteroids (ICSs)
  • Leuikotriene modifiers
  • Monoclonal antibody to IgE
193
Q

What is an example of an ICS for asthma 5

A
  • fluticasone
  • beclomethasone
  • budesonide (Pulmiocort)
  • mometasone
  • ciclesonide
194
Q

What is an example of a leuikotriene modifier 3

A
  • Montelukast (oral)
  • zafirlukast
  • zileuton
195
Q

What is an example of a monoclonal antibody to IgE

A

omalizumab (Xolair)

196
Q

What do corticosteroids do for asthma pts 5

A
  • Suppress the inflammatory response
  • Inhaled form is used in long-term control
  • Systemic form is used to control exacerbations and manage persistent asthma (methylprednisolone, Solu-Medrol IV)
  • Decrease bronchial hyperresponsiveness
  • Decrease mucous production
197
Q

What type of schedule should you take corticosteroids on

A

Fixed schedule

198
Q

What are side effects of inhaled corticosteroids. What can help with these? 3

A
  • Oropharyngeal candidiasis (yeast infection due to decrease in immune system)
  • Hoarseness
  • Dry cough
  • Using a spacer or gargling after each use can help
199
Q

What do Leukotriene modifiers do

A
  • They block the action of leukotrienes (potent bronchoconstrictors)
  • Have both bronchodilator and anti-inflammatory effects
200
Q

What is one advantage of Leukotriene modifiers

A

They can be administered orally

201
Q

What might we give in an addition to an ICS

A

Leukotriene modifiers (these do not take the place of ICSs, these are add-ons)

202
Q

What does an anti-IgE do

A
  • Decreases IgE levels
203
Q

What are IgEs

A

They’re antibodies that are released when your body overreacts to an allergen

204
Q

How is anti-IgE given

A

Subcutaneous every 2-4 weeks in a HCPs office, due to the high risk of anaphylaxis

205
Q

Describe our B-adrenergic agonists (SABAs) 4

A
  • For short acting
  • Not long-term use
  • Onset of action in minutes and last from 4-8 hrs
  • Prevent release of inflammatory mediators from mast cells
206
Q

What are side effects of SABAs (when used often - this is why you shouldn’t use often) 6

A
  • Increased HR
  • Anxiety (jittery)
  • Tremors
  • Palpitations
  • Nausea
  • Insomnia
    (be careful giving these to cardiac pts, due to the things that this drug can elevate)
207
Q

What are 2 examples of long-acting beta 2 - adrenergic agonist drugs (LABAs)

A
  • Salmeterol (Serevent)

- Formoterol (Foradil)

208
Q

Describe LABAs 3

A
  • Added to daily ICSs
  • Decrease the need for SABAs
  • Never use alone
209
Q

What is the max amount that you should be using your SABA

A

No more than twice a week

210
Q

What is a methylxanthine drug

A

Theophylline

211
Q

What is the issue with Theophylline 3

A
  • High interactions with other drugs
  • Bad side effects (GI issues, tachycardia, dysrhythmias, seizures)
  • Blood serum levels need to be regularly checked due to the safety risks
212
Q

Describe anticholinergic drugs 4

A
  • ipratropium (Atrovent)
  • Prevent muscles in the bronchi from tightening by blocking acetylcholine
  • Short-acting (not as effective as albuterol)
  • More effective for COPD
213
Q

What devices are used to inhale asthma medications

A
  • Nebulizers
  • DPIs (Dry Powder Inhalers)
  • MDI (Metered Dose Inhalers)
214
Q

What is the big thing to know about nonprescription combination drugs like epinephrine and ephedrine

A

They can be very dangerous due to their side effects. Caution pts from using these (can cause heart palpitations, dysrhythmias, tremors, insomnia, increased BP).

215
Q

Why are MDIs and spacers beneficial

A

They reduce the amount of medicine delivered to your throat and increase the amount of med delivered to your lungs.

216
Q

How should you use your inhaler 5

A
  • Shake the inhaler
  • Breathe out all the way
  • Put the inhaler to your lips and breathe in slowly
  • Hold breath for 10 seconds
  • Wait one minute between breaths for quick-relief meds (not need to wait for the others)
217
Q

What assessments are we going to do for someone with asthma 4

A
  • History
  • ABGs
  • Lung function tests
  • Physical (accessory muscles, diaphoresis, cyanosis, lung sounds)
218
Q

What is the PEFR goal

A

Maintain 80% of personal best

219
Q

What is an asthma’s pts wheezes get louder

A

It can indicate that they are having a positive response to the tx

220
Q

What can we do as nurses when a pt is having an acute asthma attack 3

A
  • Stay with them
  • Get them comfortable
  • Use “talking down” (make eye contact with them and coach them in pursed lip breathing)
221
Q

What is some good pt teaching for someone with asthma

A
  • Know when to seek medical tx
  • Use your peak flow meter daily
  • Have a written plan
  • Get good nutrition
  • Get good sleep
  • It’s also hard to pts with asthma to notice that their breathing is changing (this is why you do your peak flows - as they will indicate if something is happening when they go down)
222
Q

Describe the three peak flow zones

A
  1. Green zone: 80-100% of personal best (keep doing everything the same)
  2. Yellow zone: 50-80% of personal best (caution - something is triggering asthma - need medications - call HCP because something isn’t working)
  3. Red zone: less than 50% of best (serious problem - action must be taken with HCP)
223
Q

What are our bronchodilator drugs 4

A
  • SABA (albuterol)
  • Anticholinergics (ipratropium)
  • LABA (Serevent)
  • Methylxanthines (theophylline)
224
Q

What do bronchodilators do

A

Prevent bronchospasms by stopping the release of inflammatory mediators from mast cells
- No anti-inflammatory effects

225
Q

What hurts both the bronchi and the alveoli, COPD or asthma

A

COPD (only the bronchi are affected in asthma)

226
Q

What is the number one red flag and priority with someone having an acute asthma attack

A

The “silent chest”

227
Q

If someone is having an acute asthma attack, are we going to see prolonged inhalation or prolonged exhalation

A

Prolonged exhalation

228
Q

What ABGs are we going to see for someone in respiratory acidosis

A
  • pH less than 7.35
  • paCO2 over 45
  • paO2 less than 80 (hypoxic)
229
Q

What are the neuro signs of hypoxia 3

A
  • Agitation
  • Restlessness
  • Drowsiness
    (we will see mental status changes)
230
Q

What if someone has status asthmaticus, where drugs aren’t going to work for them

A

Intubate

231
Q

Does stress cause asthma attacks

A

Yes, it can

232
Q

How and how often do we clean albuterol MDIs vs corticosteroid MDIs

A
  • Albuterol: Rinse with warm water 1-2 times per week (doesn’t need to be cleaned after every use)
  • Corticosteroids: Wash inhaler and mouth out after every use.
233
Q

During an acute asthma attack, what drugs are we giving (think AIM)

A

A: albuterol
I: ipratropium
M: methylprednisolone (Solu Medrol)

234
Q

Can you reverse COPD

A

No, it’s a chronic, irreversible condition

235
Q

What is COPD

A

Progressive disease, where there is an abnormal inflammatory response in the lungs, which is primarily caused by cigarette smoking and other noxious particles or gases

236
Q

So what’s the relationship between chronic bronchitis and emphysema

A

Both are no longer included in the definition of COPD

  • Chronic bronchitis is now its own independent disease
  • Emphysema is something that can happen in COPD pts, where the alveoli are destroyed
237
Q

What is chronic bronchitis

A

Cough and sputum production for at least 3 months in 2 consecutive years

238
Q

What are risk factors for COPD 7

A
  • Smoking
  • Chemicals and dust
  • Pollution
  • Severe recurring respiratory infections
  • Asthma
  • Aging
  • a1-antitrypsin deficiency
239
Q

What is a1-antitrypsin deficiency

A

Autosomal recessive disorder that can put you at a genetic risk for developing COPD

240
Q

What is the purpose of a1-antitrypsin

A

It is a protein found in the lungs, that protects lung tissue from being attacked during inflammation related to smoking and infections

241
Q

How might smoking lead to COPD 4

A
  • The irritating smoke causes hyperplasia of cells, which increases mucus production, thus causing airways to become smaller
  • Decrease or lost ciliary activity
  • Abnormal distal dilation and destruction of alveoli
  • Chronic, enhanced inflammation, which leads to destruction of collagen by increasing proteolytic enzymes
242
Q

When should COPD be considered in a smoker

A

If they are over 40 and have a history of 10 or more pack-years

243
Q

How do you calculate pack-years

A

Pack per day multiplied by the years that they’ve been smoking (ie half of pack a day for 30 years would be 15 pack years)

244
Q

How many cigarettes are in a standard pack

A

20

245
Q

What are the effects of nicotine 3

A

Stimulates the sympathetic nervous system, which leads to COPD

  • Increase HR
  • Cause peripheral vasoconstriction
  • Increase BP and cardiac workload
246
Q

What is interesting about pollution and COPD

A

Many people are developing COPD, even though they have never smoked, due to poor ventilation when cooking indoors using coal and other biomass fuels

247
Q

What infections are risk factors for COPD

A

HIV and TB

248
Q

How can aging put you at risk for COPD

A

Most older adults develop emphysema due to their lungs changing (lungs becoming less elastic, chest wall stiffens - basically you’re showing signs of emphysema)

249
Q

What is happening in COPD 3

A
  • Loss of elastic recoil
  • Airflow obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm
  • Inflammation from noxious particles and gas = damage to lung tissue, inflamed airways, parenchyma destroyed (type of lung tissue)
250
Q

Do COPD have the same inflammatory cells reacting

A

No, they have different inflammatory cells reacting

251
Q

Basically, what are the 4 pathophys changes caused by noxious particles and gases

A
  • Inflammation of airways
  • Peripheral airway remodeling
  • Parenchymal destruction
  • Pulmonary vascular changes (thick vessels, capillaries destroyed, arteries vasoconstrict)
252
Q

What ends up happening in COPD 9

A
  • Mucus hypersecretion
  • Cilia dysfunction
  • Airflow limitation
  • Hyperinflation of lungs
  • Alveolar destruction
  • Loss of elastic recoil
  • Gas exchange abnormalities
  • Pulmonary hypertension
  • Cor pulmonale
253
Q

When structures in the lungs are destroyed from COPD, what do we see 3

A
  • Air goes in easily, but remains in the lungs
  • Bronchioles collapse
  • Causes barrel-shaped chest
254
Q

What would the alveoli look like in someone with COPD 2

A
  • We would see bullae and blebs (large air spaces)

- Fewer, larger alveoli

255
Q

What can these pulmonary vascular changes result in

A

Pulmonary hypertension

256
Q

What disease do we often see go with COPD

A

Cardiovascular disease

257
Q

What clinical manifestations will we see with COPD 3

A
  • Chronic cough or sputum production (usually in the morning)
  • Dyspnea
  • History of risk factors
258
Q

How is dyspnea working with COPD

A

It comes on slowly, people may ignore it and state that they’re just “out of shape,” then it starts to get worse and interfere with their ADLs, then they start to have it even while at rest

259
Q

Why does a COPD pt have chest breathing with COPD

A

The overinflated lungs have caused the diaphragm to flatten to accommodate the lungs. This forces the pt to become a chest breather, because they are relying more on intercostal and accessory muscles

260
Q

What are some other clinical manifestations of COPD 5

A
  • Chest breathing
  • Wheezing and chest tightness
  • Underweight and anorexic
  • Chronic fatigue
  • Paroxysmal coughing that is so severe that it may cause a pt to faint or fracture their ribs
261
Q

What might we see if we examined someone with COPD 7

A
  • Prolonged expiratory phase
  • Wheezes
  • Decreased breath sounds
  • Increase in anterior-posterior diameter (barrel chest)
  • Tripod position
  • Pursed lip breathing
  • Polycythemia (thickening of RBCs) and cyanosis
262
Q

What does polycythemia and cyanosis look like? 6

A
  • Hypoxemia (PaO2 less than 60 or SaO2 less than 88%)
  • Hypercapnia (PaCO2 over 45)
  • Increased production of red blood cells
  • Bluish-red color of skin
  • Hemoglobin concentrations my reach 20 g/dL
  • Might see right-sided edema (indicates cor pulmonale
263
Q

Why does polycythemia occur

A

Your body is trying to compensate by producing more RBCs when you are experiencing chronic hypoxemia

264
Q

What could we use to determine the degree of COPD, and what would we find 2

A
  • You could use a FEV1/FVC test . Less than 70% indicates COPD.
  • You could also see an increased residual volume (they can take in air, but they can’t get the air out)
265
Q

Besides an FEV1/FVC test, what other diagnostic tests could you do to determine if someone has COPD 4

A
  • Chest x-ray
  • 6 minute walk test
  • COPD Assessment Test (CAT)
  • Clinical COPD Questionnaire (CCQ)
  • ABGs
  • Echocardiogram or multigated acquisition (MUGA) (cardiac blood pool) scan (look at heart function)
  • Sputum for culture and sensitivity (for infection purposes)
266
Q

What is a normal SaO2 reading for a pt with COPD

A

They usually live at or below 88%

267
Q

What would you see on a chest x-ray that would indicate COPD

A

A flat diaphragm because of the hyperinflated lungs

268
Q

Why would we get a culture and sensitivity for our COPDers

A

They tend to get chronic lung infections, like MRSA

269
Q

What ABGs would we see for someone with late stage COPD 4

A
  • Low PaO2
  • Increased PaCo2
  • Decreased pH
  • Increased HCO3 (kidneys are trying to keep bicarbonate to help increase pH)
270
Q

What are COPD complications 5

A
  • Pulmonary hypertension which leads to cor pulmonale
  • Exacerbations of COPD
  • Acute respiratory failure
  • Peptic ulcer disease
  • Depression/anxiety
271
Q

What is pulmonary hypertension

A

Constriction of the pulmonary vessels in response to alveolar hypoxia (Basically the blood vessels in the lungs are working super hard)

272
Q

Do all COPD pts develop cor pulmonale

A

No

273
Q

Is Cor pulmonale an early or late stage manifestation of COPD

A

Late stage

274
Q

How does pulmonary hypertension lead to cor pulmonale

A

Now that the blood vessels are working super hard in the lungs due to the hypertension, this has caused pressure to increase on the right side of the heart, as it is working harder to push blood into the lungs. This increase in pressure leads to right sided heart failure.

275
Q

What are signs and symptoms of cor pulmonale 5

A
  • Dyspnea, possible lung crackles
    (the below symptoms are all signs of right sided heart failure)
  • Distended neck veins
  • Hepatomegaly with right upper quadrant tenderness (enlarged liver with pain)
  • Peripheral edema
  • Weight gain
276
Q

What diagnostic studies can you do to determine if someone has cor pulmonale 4

A
  • Chest x-ray (large pulmonary vessels)
  • Right sided cardiac catheterization (increased pressure)
  • Echocardiogram (show right sided heart enlargement)
  • BNP levels (shows heart failure)
277
Q

How do we manage cor pulmonale

A

Continuous O2 and diuretics

278
Q

What are COPD exacerbations

A

When someone with COPD is all of a sudden having pretty bad symptoms like increases in dyspnea, cough, sputum.
- Also look for other signs like malaise, insomnia, fatigue, depression, confusion, decreased exercise tolerance, increased wheezing or fever

279
Q

When someone is having a COPD exacerbation, what should a nurse do 7

A

Determine the severity

  • Are they using their accessory muscles
  • Do we see cyanosis
  • Do we see edema
  • Is their BP unstable
  • Are they alert
  • Does their ABGs indicate respiratory acidosis
  • Altered alertness
280
Q

What are the primary causes of COPD exacerbations

A
  • Bacterial and viral infections (increase in mucus production)
281
Q

What treatments can we give for COPD exacerbations 4

A
  • Short-acting bronchodilators
  • Oral systemic corticosteroids (can be metered dose inhaler or nebulizer)
  • Antibiotics
  • Supplemental oxygen therapy
282
Q

How can COPD cause acute respiratory failure 4

A
  • Discontinuing bronchodilator or corticosteroid medication
  • Overuse of sedatives, benzos and/or opioids (these can worsen your RR)
  • Surgery or or severe, painful illness involving the chest or abdomen (just don’t get enough air)
  • Exacerbations (Typically COPD pts wait too longer to contact HCP when they have fever, increase cough, dyspnea or other exacerbation symptoms)
283
Q

If a COPD pt becomes anxious, what can we teach them to do

A

Pursed lip breathing

284
Q

How do we teach someone to do pursed lip breathing 4

A
  • Inhale slowly and deeply through the nose
  • Exhale slowly through pursed lips, as if whistling
  • Do not puff out your cheeks
  • Making breathing out 3 times a long as breathing in
285
Q

What might we see being given for anxiety and depression for our COPD pts

A

buspirone (BuSpar) — Never give benzos due to decrease in RR and habit forming

286
Q

How will we tx a stable COPD pt 4. What will we evaluate and discuss with them?

A
  • As outpatient (only hospitalized for exacerbations and respiratory failure)
  • Evaluate for environmental or occupational irritants
  • Discuss the flu and pneumococcal vaccines
  • Discuss smoking cessation
287
Q

What is the biggest thing you can do to lower your risk of developing and slowing down COPD

A

Smoking cessation

288
Q

What drugs are we giving for someone with COPD

A

Bronchodilators

  • B2 adrenergic agonists
  • Anticholinergics
  • Methylxanthines
289
Q

How will bronchodilators help someone with COPD

A
  • Relax smooth muscles in the airways
  • Improve ventilation of the lungs
  • Decrease dyspnea and increase FEV1
    (usually inhaled)
290
Q

Would we ever use a “step down” approach in medications with COPDers

A

No, because unlike asthma, COPD will continuously get worse, so they will “step up”

291
Q

What short acting drugs will we probably give for COPD

A

Albuterol (SABA) or ipratropium (anticholinergic) (either together (combivent) or alone)

292
Q

For moderate COPD, what medications are we probably using

A

LABA like salmeterol and formoterol

293
Q

When would theophylline be used

A

When pts aren’t responding with other treatments. We don’t want to use this med often, because it can interact with other meds

294
Q

What specific antibiotic may we give for someone with COPD. Why

A

Azithromycin, because it has anti-inflammatory effects and anti-mucus effects (they may take it orally everyday for this reason)

295
Q

What is an oral drug that may be given for COPD. How does it work

A

Roflumilast (Phosphodiesterase inhibitor) (helps suppress the immune response and the production of O2 radicals)

296
Q

What is different from COPD and asthma in terms of SABAs and LABAs

A

In asthma, a pt is always using SABAs and LABAs as dual therapy. However, in COPD, the pt can use LABAs only as a monotherapy

297
Q

What is kind of the drug therapy pattern with COPDers

A
  • Mild COPD/fewer symptoms = Short actings are used like albuterol and ipratropium (probably given as a combivent)
  • Moderate COPD = using LABAs, like formoterol and salmeterol (SABA may or may not still be used for acute attacks)
  • Severe COPD = ICS with a LABA combination like fluticasone/salmeterol or budesonide/formoterol
298
Q

What are our oxygen goals for COPD pts

A
  • Keeping SaO2 at least at 90% or above during all activities (sleep, rest, exertion) (you might also see a goal to keep above 88%)
  • PaO2 at least above 60 mm Hg
299
Q

What are the two methods of O2 delivery for COPDers

A
  • Low-flow (most common), mixed with room air, less precise than high-flow
  • High-flow using a venturi mask
300
Q

To prevent the drying out and irritating effects of dry O2 delivery systems, what can be used to help

A

Can use nebulizers, vapotherm or bubble-through humidifiers (these attach to the O2 delivery device)

301
Q

What are the complications from oxygen therapy 5

A
  • Combustion
  • CO2 narcosis (COPDer’s bodys are use to having high amounts of CO2, so you could cause damage by giving them oxygen and throwing off that balance)
  • O2 toxicity (high concentrations can cause an inflammatory response because of O2 free radical damage)
  • Infection (humidifiers and nebulizers can have bacteria growth)
  • Absorption atelectasis
302
Q

What is the common bacteria that effects COPD pts due to humidifiers and nebulizers (it is also resistant)

A

Pseudomonas aeruginosa

303
Q

What two things does chronic O2 therapy at home reduce

A
  • Hematocrit

- Pulmonary hypertension

304
Q

What therapies can we do for COPDers 5

A
  • Breathing retraining
  • Effective coughing
  • Chest physiotherapy (percussion, vibration, postural drainage)
  • Airway clearance devices (ie the flutter, acapella)
  • High-frequency chest wall oscillation (a vest that vibrates the chest)
305
Q

What is the purpose of pursed lip breathing for COPDers 4 and what does it teach

A
  • Prolongs exhalation
  • Prevents bronchiolar collapse and air trapping
  • Helps eliminate CO2
  • Teaches pt to use “just enough” positive pressure
306
Q

How do you use your peak flow meter (for asthma) 4

A
  • Take a deep breath
  • Blow on the mouth piece as hard and as fast as you can
  • Record your number
  • Repeat two mor times and write down your best number out of the three
307
Q

Besides pursed lip breathing, what is another good breathing technique to teach for COPDers. What is good, what is bad

A

Diaphragmatic breathing

  • Good because it teaches you to use your diaphragm instead of accessory muscles
  • Helps achieve maximum inhalation and slows the RR
  • Bad: may increase the workload of breathing and cause dyspnea
308
Q

What is a different type of coughing technique you can teach your COPD pts

A

Huff coughing (forces secretions into your larger airways)

309
Q

Talk more about postural drainage for COPDers 5

A
  • Tx is individualized
  • Usually ordered 2-4 times per day
  • In position for 5 minutes with percussion and vibration being used
  • Done 1 hr before meals and 3 hrs after meals
  • Cannot be used on unstable pts (traumatic brain injury, chest trauma, hemoptysis, heart disease, pulmonary embolus)
310
Q

Discuss a flutter mucus clearance device

A
  • Provides positive expiratory pressure (PEP) tx

- When pt blows on the device, it produces vibrations in the lungs to loosen up the mucus

311
Q

When thinking about our COPD pts, what is our biggest goal of therapy

A

Clearing those secretions

312
Q

What describes malnutrition in COPDers 3

A

It is multifactorial (caused by a lot of different things)

  • Increased inflammatory mediators
  • Increased metabolic rate (from ventilatory effort - using more energy to breathe)
  • Lack of appetite
313
Q

What is some pt teaching that we can provide to help decrease dyspnea and conserve energy when eating 6

A
  • Rest at least 30 minutes before eating
  • Avoid exercise for 1 hr before and after eating
  • Use bronchodilator
  • Use supplemental O2
  • Eat high-calorie, high-protein diet
  • Eat five-6 small meals a day to avoid bloating and early satiety
314
Q

What are the 4 diff types of surgical interventions you can have for COPD

A
  • Lung volume reduction surgery (LVRS)
  • Bronchoscopic lung volume reduction surgery
  • Bullectomy (to remove air pockets)
  • Lung transplantation
315
Q

What is happening in lung volume reduction surgery (LVRS)

A
  • Removing diseased lung to enhance performance of the remaining healthy lung
  • Results in decreased airway obstruction and increased room for remaining normal alveoli to expand
316
Q

What is happening in a bronchoscopic lung volume reduction surgery

A
  • One way valves are placed into the airways leading to the diseased parts of the lungs
  • Collapses a certain segment of the lung
  • Results in decreased airway obstruction and allows the remaining lung to function
317
Q

What is happening in a bullectomy

A

Large bullaes (air sacs from destroyed alveoli) are removed

318
Q

What drug, if possible, should not be given to COPDers. why

A

Nonselective beta blockers, because they can block lung receptors

319
Q

What co-morbidities can make COPD complicated for our geriatrics

A
  • Cardiovascular disease
  • Serious infections
  • Osteoporosis
  • Psychologic problems (reduced lean body mass, decreased respiratory muscle strength, increased dyspnea, lower exercise tolerance)
  • Impaired cognition
  • Lung cancer
320
Q

What is a good exercise regimen to teach COPDers

A

Walk 15-20 minutes a day at least 3 times a week with gradual increases

321
Q

What can help COPDers with sleep

A

Nasal saline sprays, decongestants, nasal steroid inhalers

322
Q

What do we need to worry about with decongestants

A

They can increase BP, so just be aware

323
Q

What are serious topics of discussion for COPDers

A

Discussing palliative, end-of-life care, hospice and advanced directives

324
Q

What is the most modifiable risk factor in the development of cardiovascular disease

A

Hypertension

325
Q

Once you have high BP, what are you more at risk for 4

A
  • MIs
  • Heart failure
  • Stroke
  • Renal disease
326
Q

What is elevated BP

A

120-129/80

327
Q

What is the BP for stage 1 hypertension

A

130-139/80-89 (either)

328
Q

What is the BP for stage 2 hypertension

A

140/90 (either)

329
Q

What is the BP for hypertensive crisis

A

180/120 (either)

330
Q

What two functions determine BP

A

Cardiac output multiplied by systemic vascular resistance

331
Q

What is cardiac output

A

The amount of blood being pumped out of the heart per minute

332
Q

What is systemic vascular resistance (SVR)

A

Force stopping blood from pumping (ie narrow arteries)

333
Q

What is the pathway of blood in the heart

A
  • deoxygenated blood flows from the right atrium to the right ventricle where it goes to the lungs to get oxygen
  • Oxygenated blood flows from the lungs to the left atrium, to the left ventricle where it is pumped out through the aorta
334
Q

What system kicks in when your BP drops

A

Your sympathetic nervous system, which tells your heart to speed out and increase contractility, causes vasoconstriction and renin release (renin increases your BP), which then increases CO and SVR

335
Q

How do baroreceptors influence BP

A

They are sensitive to the stretching of of blood vessels. So when they are stimulated by an increase in BP, they send signals to the sympathetic vasomotor center to stop, which results in a decrease in HR, force of contraction and vasodilation. When they sense a fall in BP, they tell the SNS to get their butt in gear, which leads to constriction, increased HR and increased contractility of the heart.

336
Q

How does hypertension affect baroreceptors

A

The baroreceptors become adjusted to elevated BP levels and recognize this level as their new “normal”

337
Q

How does vascular endothelium cells play a role in controlling BP

A

These cells maintain dilation and constriction

338
Q

What two things can damage endothelium cells

A
  • Smoking

- Diabetes

339
Q

How can the kidneys impact BP 3

A
  • Control of sodium
  • RAAS system
  • Prostaglandins
340
Q

How does sodium control impact BP

A

The kidneys are responsible for excreting sodium. If they don’t excrete enough sodium, then more sodium stays in the body. Water follows sodium, so you will have an increase in fluid. This increase in fluid causes the pressure in the body to increase, resulting in high BP

341
Q

How does the RAAS system impact BP

A

The kidneys will secrete renin when there is a decrease in blood flow through the kidneys or a decrease in sodium concentration. Renin then converts agiotensinogen to angiotensin I, which is then converted to angiotensin II via ACE enzyme. This angiotensin II increases BP by vasoconstriction, which increases the SVR, and this results in an immediate increase in BP. Then over a period of hours or days, it increases BP indirectly by stimulating the adrenal cortex to secrete aldosterone.

342
Q

How do prostaglandins impact BP

A

They cause vasodilation

343
Q

What endocrine hormones come into play with BP 3

A
  • Epinephrine and norepinephrine
  • Aldosterone
  • ADH
344
Q

How does epinephrine and norepinephrine influence BP

A

Increases CO by increasing HR, myocardial contractility and vasoconstriction of peripheral arterioles

345
Q

How does aldosterone influence BP

A

It tells your kidneys to keep sodium, which then causes your body to keep water, which then causes your BP to go up due to the increase in fluid volume

346
Q

How does ADH influence BP

A

It tells your body to retain water, which will increase blood volume and cardiac output

347
Q

What is primary hypertension

A

Hypertension without an identified cause, but there are multiple contributing factors (most common)

348
Q

What are risk factors for primary hypertension (there’s a bunch)

A
  • Age (vessels lose their elasticity)
  • Alcohol (releases renin which causes your vessels to constrict)
  • Smoking (vasoconstrictor)
  • DM (damages arteries)
  • Elevated serum lipids
  • Excess dietary sodium
  • Gender (women are higher after menopause)
  • Family History
  • Obesity (heart has to work harder)
  • Ethnicity
  • Sedentary lifestyle
  • Socioeconomic status (education level)
  • Stress
349
Q

What should be the max number of alcoholic drinks per day

A

No more than 3

350
Q

What is the hallmark of primary hypertension

A

Persistently increased system vascular resistance (SVR)

351
Q

What can lead to the development of primary hypertension 6

A
  • Genetics
  • Water and sodium retention
  • Stress and increased SNS activity
  • Altered RAAS
  • Insulin resistance
  • Endothelial dysfunction (heart cells)
352
Q

What is the genetic link with sodium and primary hypertension

A

People can eat the same amount of sodium, but only some will get hypertension from it. This indicates a genetic link, where some people are more sensitive to sodium then others

353
Q

How does insulin resistance lead to primary hypertension

A

High insulin levels can stimulate the SNS and cause vasodilation, vascular hypertrophy (thickening of muscle) and increase sodium reabsorption

354
Q

What is secondary hypertension

A

Caused by something specific

355
Q

How do you treat secondary hypertension

A

Remove/fix the cause

356
Q

What are causes of secondary hypertension 8

A
  • Coarctation of aorta (narrow aorta due to birth defect)
  • Renal disease (where you’re getting low blood volume to the kidneys, which then forces your kidneys to retain sodium, which leads to fluid retention)
  • Endocrine disorders (hormone imbalances, pituitary, aldosterone, hyperthyroidsm makes your HR increase, hypothyroidism makes HR less efficient, cushings)
  • Neurologic disorders (tumors)
  • Cirrhosis (portal vein will get backflow)
  • Pregnancy (ie having multiples, being older, etc)
  • Sleep apnea (brain increases HR and BP during sleep apnea to try and save you when you stop breathing)
  • Various drugs (ie meth - increase HRs, estrogen)
357
Q

What is unique about the symptoms of hypertension in the beginning

A

It is known as the “silent killer” because there usually aren’t any symptoms

358
Q

What are symptoms of severe hypertension (hypertensive crisis) 7

A
  • Fatigue
  • Dizziness
  • Palpitations
  • Angina
  • Dyspnea
  • Nosebleeds
  • Anxiety
359
Q

What are complications of hypertension 5

A

When organs start to be impacted by hypertension, this includes:

  • heart
  • brain
  • peripheral vascular disease (vessels)
  • kidney
  • eyes
360
Q

What kinds of things can happen to your heart from hypertension 3

A
  • Coronary artery disease (narrowing of arteries, hardening of arteries)
  • Left ventricular hypertrophy (heart is working so hard)
  • Heart failure (these lead to heart failure - heart can’t take anymore)
361
Q

What are symptoms of HF 2

A
  • SOB, especially at night

- Fatigue

362
Q

How can hypertension damage the brain 2

A
  • High BP can cause cerebral edema, which is intercranial pressure
  • Stroke
363
Q

How can your eyes be impacted by hypertension

A

We can see damage to the vessels from the increase in pressure

364
Q

How should we measure BP 2

A
  • Take two or more readings at separate occasions in a consistent manner (ie same time of the day, same sitting position)
  • Measure BP on both arms for the first time to determine the diff., use the higher reading after that.
365
Q

What diagnostic is usually ordered for hypertension evals. Why

A

Ambulatory blood pressure monitoring (ABPM)
- Helps determine a more accurate BP incase someone is having “white coat” hypertension (from being in the doctors office)

366
Q

How does ABPM work

A

Automated system that measures BP at intervals over a 12-24hr period.

  • Record activities and reading in diary
  • Keep arm still by their side when monitor is trying to get a reading
367
Q

Once BP is stable, how often will it be checked

A

Once every 3-6 months to see how they are responding to tx

368
Q

What diagnostic assessments (besides ABPM) are we doing for hypertension (there’s a lot)

A
  • UA
  • BUN/creatinine
  • Creatinine clearance
  • Electrolytes
  • Glucose
  • Lipids
  • Uric acid levels (want baseline, because diuretic therapy will increase uric acid levels)
  • CBC
  • Thyroid function
  • LFTs
  • ECG
  • Echo
  • Ophthalmic exam
369
Q

What pt teaching can we give to help modify lifestyle factors of hypertension 7

A

“Life’s simple 7”

  • Manage BP
  • Control cholesterol
  • Reduce blood sugar
  • Get active
  • Eat better
  • Lose weight
  • Stop smoking
370
Q

A weight reduction by how many pounds may decrease SBP by approx. 5-20mm Hg

A

22lbs (10kg)

371
Q

What does the DASH diet help you do

A

Lower BP and LDLs

372
Q

What things are they eating on a DASH diet 9

A
  • Fruits
  • Veggies
  • Fat-free/low-fat milk
  • Whole grains
  • Fish
  • Poultry
  • Beans
  • Seeds
  • Nuts
373
Q

What is the max amount of sodium intake for the average adult

A

2300mg or less

374
Q

What is the max amount of sodium intake for a high risk pt

A

1500mg or less

375
Q

What is the recommended amount of moderate-intensity aerobic activity per week (if they don’t do vigorous)

A

150 min/week

376
Q

What is the recommended amount of vigorous-intensity aerobic activity per week (if they don’t do moderate)

A

75min/week

377
Q

How often should you do muscle-strengthening and flexibility and balance exercises

A

2 times a week

378
Q

How many drinks put you at risk for hypertension

A

3 or more

379
Q

What is the alcohol limit for men and women

A

Men should have no more than 2 drinks/day and women should have no more than 1 drink/day

380
Q

When can pts notice changes in their cardiovascular health after they stop smoking

A

They can notice changes within 1 year

381
Q

What do ACE inhibitors end in

A

Pril

382
Q

What do ARBs end in

A

sartan

383
Q

What do alpha blockers end in

A

osin or zosin

384
Q

What do beta blockers end in

A

lol

385
Q

What do calcium channel blockers end in

A

dipine

386
Q

What do diuretics end in

A

ide

387
Q

How do ACE inhibitors work

A

They prevent the conversion of angiotensin I to angiotensin II (angiotensin II causes vasoconstriction and sodium and water retention)

388
Q

What is an ACE inhibitor drug

A

Lisinopril

389
Q

What are some nursing considerations to remember about ACE inhibitors 4

A
  • NSAIDs and aspirin may reduce effectiveness
  • Can use with diuretics, except potassium sparing diuretics
  • Can increase creatinine levels (because they can decrease blood flow to kidneys, which can lead to kidney damage)
  • Pts may have a dry, hacking cough
390
Q

What should you remember about lisinopril 3

A
  • You can have angioedema (everything swells, notably the lips and tongue)
  • Dry, cough
  • Hyperkalemia
391
Q

How do angiotensin II receptor blockers (ARBs) work

A

They block angiotensin II from binding to receptors in the walls of blood vessels

392
Q

What is the most common ARB prescribed

A

losartan

393
Q

What are some nursing considerations for ARBs 3

A
  • Teach pts it may take 3-6 weeks to see full effects
  • Will usually be given instead of ACE inhibitors when pts have a dry cough from ACE inhibitors
  • Do not combine with ACE inhibitors due to adverse renal effects
394
Q

How do alpha blockers work

A

They block alpha1 receptors on blood vessels, thereby preventing sympathetic catecholamines such as norepinephrine and epinephrine from binding. This causes decreased vasoconstriction and blood pressure. (Basically, they stop the fight or flight response from the SNS)

395
Q

What is the more common alpha blocker

A

Prazosin

396
Q

What are some nursing considerations for alpha blockers 2

A
  • Teach pts to take at bedtime to reduce risks associated with orthostatic hypotension
  • Teach pts to change positions slowly due to orthostatic hypotension
397
Q

How do beta blockers work

A

Block beta 1 receptors in the heart, thereby preventing sympathetic catecholamines such as norepinephrine and epinephrine from binding. This causes a decrease in HR, stroke volume, CO and BP.

398
Q

What is the diff between alpha and beta blockers

A

The receptors in beta blockers are actually located in the heart, whereas alpha receptors are located in blood vessels

399
Q

What are 3 common beta blockers

A
  • Atenolol
  • Metoprolol
  • Propranolol
400
Q

What are nursing considerations for beta blockers 6

A
  • Monitor BP and pulse regularly
  • Use with caution in diabetics (can suppress tachycardia related to hyperglycemia and it can effect glucose metabolism)
  • Drug of choice for pts with history of MI/HF
  • Less effective in African American pts
  • Esmolol IV only
  • May cause bronchospasm in pts with asthma ( do not give)
401
Q

What might be good to take with someone who is taking metoprolol

A

Their apical pulse

402
Q

How do calcium channel blockers work

A

They block the calcium channels of vascular smooth muscle cells on the cardiac cells, which decreases smooth muscle contraction, vasoconstriction and blood pressure

403
Q

What are the two main types of calcium channel blockers. What’s the diff.

A

Dihydropyridines (more common, because they’re more effects) and non-dihydropyridines. Dihydropyridines effect blood vessels, while non-dihydropyridines effect the heart

404
Q

So what does calcium do when it enters these cells

A

It causes contraction and constriction, so if you block these channels, you could decrease contraction and constriction = lowers BP

405
Q

What is the most common calcium channel blocker

A

Amlodipine

406
Q

What are nursing considerations for calcium channel blockers

A
  • Be aware they are more potent vasodilators, so be careful mixing with other vasodilators
  • Clevidipine is for IV use only
  • Only use IV nifedipine for emergencies
  • Serious effects have occurred, like MIs and CVAs
407
Q

How do diuretics work

A

They stop the reabsorption of sodium, which causes water to follow sodium out of the body, which decreases BP

408
Q

What are the 3 main types of diuretics

A
  • Loop diuretics
  • Thiazide diuretics
  • Potassium sparing diuretics
409
Q

What is the most common loop diuretic. And what should you monitor

A

Furosemide. Monitor for orthostatic hypotension and electrolyte imbalances

410
Q

What is the most common thiazide diuretic, and what should you monitor

A

Hydrochlorothiazide. Monitor for hypotension and hypokalemia. May need potassium supplements. Also, reducing sodium can help reduce the risk for hypokalemia.

411
Q

What is the most common potassium sparing diuretic, and what should you watch for.

A

Spironolactone. Monitor for orthostatic hypotension, hyperkalemia. Do not give to someone with renal failure. Avoid potassium supplements.

412
Q

What drugs do you want to avoid with potassium sparing diuretics

A

ACE inhibitors or ARBs, because they can cause hyperkalemia

413
Q

What are the only 2 drugs that lower both SVR and SV

A

ACE inhibitors and ARBs (so they work on both decreasing how often the heart pumps (SV) and decrease resistance in the vessels (SVR))

414
Q

What are the only 2 drugs that lower SVR only

A

Alpha blockers and calcium channel blockers

415
Q

What is the only drug that lowers HR and SV

A

Beta blockers

416
Q

What is the only drug that lowers SV only

A

Diuretics

417
Q

What is a good way to remember the names of our ACE inhibitors suffix

A

Think of April (A for ACE and the suffix “pril” for our drugs)
Or you gambled away your “pril” necklace playing cards

418
Q

What is a good way to remember the ARBs suffix

A

Both ARBs and the suffix “sartan” have AR in it

419
Q

What is a good way to remember alpha blocker ssuffix

A

Alphas will be the first to get to the “osin”

420
Q

What is a good way to remember calcium channel blockers suffix

A

Happy cows live in California, and California has a lot of “PINE” trees

421
Q

What is a good way to remember diuretics suffix

A

You want to h”ide” from your pt when they have diuretics, because they will need to pee a lot

422
Q

What is some good pt teaching in regards to hypertensive drugs 4

A

Encourage the pt to report all side effects such as

  • Orthostatic hypotension
  • Sexual dysfunction (common with these drugs)
  • Dry mouth (diuretics)
  • Frequent urination (diuretics)
423
Q

What is dangerous about sexual dysfunction and hypertensive drugs

A

Sexual dysfunction may cause males to stop taking their meds, which can be very dangerous. Have them notify their HCP, who can help with switching to another med that may not cause this problem

424
Q

How do you measure BP for orthostatic hypotension 3

A
  • Take BP and pulse when pt is supine, sitting and standing
  • Measure within 1-2 minutes of position changes
  • Pt has orthostatic hypotension if their SBP drops 20 points, if their DBP drops 10 points or if their HR increases by 20 beats
425
Q

How does aging affect your risk for developing hypertension 3

A
  • You have altered drug absorption, metabolism and excretion
  • Increased risk of orthostatic hypotension due to low volume, decreased renal/hepatic function and electrolyte imbalances (basically not taking in enough fluids)
  • Postprandial drops in BP, where their BP drops about 1 hour after eating and then returns 3-4 hrs after eating (this can lead to orthostatic hypotension)
426
Q

What BP indicates a hypertensive crisis

A

BP over 180/120 (can even be 240/140)

427
Q

What are the two types of hypertensive crisis

A
  • Hypertensive urgency (no evidence of target organ disease)
  • Hypertensive emergency (target organ disease, usually requires hospitalization)
428
Q

What can hypertensive emergencies lead too 7

A
  • Encephalopathy (brain damage)
  • Intracranial or subarachnoid hemorrhage
  • HF
  • MI
  • Renal failure (not getting enough blood flow to the kidneys)
  • Dissecting aortic aneurysm (the aorta is torn)
  • Retinopathy
429
Q

What if hypertensive emergencies go untreated

A

Most people will die within 1 year

430
Q

What things can increase your risk of having a hypertensive emergency

A
  • Not taking your meds as prescribed

- Doing drugs like crack and cocaine

431
Q

What are symptoms of hypertensive encephalopathy 6

A
  • Severe headache
  • nausea
  • Vomiting
  • Seizures
  • Confusion
  • Common
    (these symptoms are caused by cerebral edema and disruption of cerebral function)
432
Q

What are symptoms of an aortic dissection

A

Severe chest and back pain with reduced or absent pulses in extremities

433
Q

When someone is having a hypertensive emergency, do we treat based on their BP

A

No, treat based on their MAP (mean arterial pressure)

434
Q

If the pt is stable in their hypertensive emergency, how should we lower their BP. What happens if we do it too quickly

A

Slowly, over a 24hr period. If it’s too quick, it can cause a decrease in perfusion to organs, and may cause a stroke, MI or renal failure.

435
Q

Do hypertensive urgency cases need IV therapy

A

No, they are usually treated with oral hypertensives

436
Q

How do you calculate the MAP

A

(SBP+2DBP)/3

437
Q

What do most people need their MAP to be in order to have adequate perfusion. What is normal

A

At least 60. Usually anything between 70-100.

102 (5 decks)

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