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RCP > RCP 103 midterm > Flashcards

RCP 103 midterm Flashcards

1
Q

Peripheral chemoreceptors

A

oxygen induced cell that react to a reduction of oxygen in the arterial blood (PaO2)
- most active below 60% PaO2
- suppressed when PaO2 falls below 30%

*when PaCO2 is HIGH/ PaO2 LOW –> peripheral chemoreceptors are primary receptor sites to control ventilation (emphysema)
- also stimulated by DECREASED pH

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2
Q

Hypoxemia

A

caused by DECREASED v/q ratio, pulmonary shunting, venous admixture

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3
Q

Central chemoreceptors

A

DRG/VRG are responsible for coordination of respiration stimulation by H+ ions in the CSF

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4
Q

Deflation reflex

A

compressed/deflated lungs (atelectasis)= INCREASED RR

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5
Q

Hering-Breuer

A

when receptors are stretched (during deep inspiration) reflex response is triggered to decreased the ventilatory rate
- does NOT occur when temperature is LOW

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6
Q

Irritation reflex

A

when the lungs are exposed to irritants, compressed, deflated irritant receptors are stimulated
- RR, cough, bronchospams INCREASE

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7
Q

Juxtapulmonary-capillary receptors (J receptors)

A

when stimulated –> reflex triggers rapid, shallow breathing

Activated= pulmonary capillary conjestion, capillary hypertension, edema of alveolar walls, humoral agents (serotonin), lung deflation, emboli in pulmonary microcirculation

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8
Q

Reflex from cartoid/aortic snius baroreceptors

A

activation causes DECREASED HR, RR –> INCREASED systemic blood pressure

INCREASED HR, RR –> DECREASED systemic blood pressure

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9
Q

Autonomic Nervous System

A

Regulates involuntary functions (heart rate, smooth muscle, and glands)

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10
Q

Sympathetic NS

A

Accelerates cardiac rate, constricts blood vessels, relaxes bronchial smooth muscle, and raises B/P

Neurotransmitters: epinephrine & nor-epinephrin

These agents stimulate alpha receptors (arterial smooth muscle constriction) beta2 receptors (bronchial smooth muscle relaxation)

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11
Q

Parasympathetic NS

A

Slows heart rate, constricts bronchial smooth muscle, increases intestinal peristalsis, and gland activity

Acetylcholine is released when the parasympathetic system is stimulated

Causes bronchial smooth muscle constriction

Beta2 blockers, i.e., propranolol

Parasympathetic blocking agent : atropine

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12
Q

Respiratory zone

A
  • type 1 cells for STRUCTURE
  • type 2 cells (PRODUCE SURFACTANT)
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13
Q

FVC

A

= maximum volume of gas that can be exhaled as forcefully and rapidly as possible after a maximal inspiration

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14
Q

FEV1/FEV ratio

A

= comparison of the amount of air exhaled in 1 second to the total amount exhaled during the FVC maneuver

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15
Q

FVC, FEV1, FEV1/FEV ratio

A

= used to differentiate between an obstructive and restrictive lung disease and to determine the severity of the patient’s pulmonary disorder

FEV1 decreased= obstructive

FEV1 increased or normal= restrictive

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16
Q

Respiratory Failure

A

PaO2= less than 60mmHg
PaCO2= greater than 50mmHg

Acute → high PaCo2, low pH

Chronic → high PaCO2, normal pH
- Restrictive lung disorders
- chronic obstructive disorders
- neonatal/early respiratory disorders

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17
Q

Hyperventilation

A
  • Asthma
  • COPD
  • Drug overdose

Acute ventilatory failure
pH= 7.25 (acid)
PCO2= 50 (high)
PAO2= 75 (low)
- HCO3 increases → PACO2 in blood → increase PCO2 , HCO3 levels

Acute alveolar hyperventilation
pH= increased
PAO2= decreased
HCO3= decreased or normal
PACO2=decreased
- Increase PH increase PAO2 increase HCO3 decrease PCO2

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18
Q

Superimposed

A
  • acute shunt disease like pneumonia/pulmonary edema

Acute alveolar hyperventilation superimposed on chronic ventilatory failure
pH= increased
PaCo2= increased
HCO3-= high increased
PaO2= decreased

Acute ventilatory failure superimposed on chronic ventilatory failure
pH= decreased
PaCO2= high increased
HCO3-= high increased
PaO2= decreased

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19
Q

Normal ABGs

A

pH= 7.35-7.45
PaCO2= 35-45
PaO2= 80-100
HCO3-= 22-28

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20
Q

Respiratory Alkalosis

A

pain
hypoxia
anxiety

pH= high
PaCO2= low
HCO3-= normal

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21
Q

Metabolic alkalosis

A

diuretics

pH= high
PaCO2= normal
HCO3-= high

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22
Q

Metabolic acids

A

diabetes

kidney condition

pH= low
PaCO2= normal
HCO3-= low

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23
Q

Compensated

A

COPD
chronic bronchitis
emphysema
restrictive lung diseases

Chronic alveolar hyperventilation is completely compensated
pH: 7.43 (normal)
PaCO2: 31 (below)
HCO3: 22 (normal)
PaO2: 74 (low)

Chronic ventilatory failure
pH= normal
PaCO2= increased
HCO3-= big increase
paO2= decreased

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24
Q

Obstructive lung disease

A

INCREASE airway resistance (Raw) → INCREASE time constant= asthma, chronic bronchitis, emphysema, cystic fibrosis

RV, Vt, FRC increased
VC, IC, IRV, ERV decreased

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25
Q

Restrictive lung disease

A

DECREASE lung compliance (CL) → DECREASE time constant= atelectasis, pneumonia, pneumothorax, pleural effusions, pulmonary edema, acute respiratory distress syndrome, interstitial lung disease

VC, IC, RV, FRC, Vt, TLC decreased

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26
Q

Bronchopulmonary Hygiene therapy protocol

A

enhance mobilization of bronchial secretions

Restore mucociliary blanket
Hydrate and remove retained secretions
Improve cough effectiveness
Prevent/treat atelectasis

-> PT meet indications for airway clearance
-> meet indications for bland aerosol
-> heated/cool aerosol
-> PT LOC
-> can PT use mouthpiece
-> access outcomes
-> therapy objectives met

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27
Q

Lung expansion protocol

A

to prevent or treat alveolar consolidation and atelectasis

predisposing conditions for atelectasis
upper abdominal/thoracic surgery
surgery in patients with chronic lung diseases and CHF
excessive secretions
chronic neuromuscular conditions

—> PT meet indication for therapy
→ patient alert and IC greater than 35%
→ discontinue or re-evaluate patient therapy assessment protocol

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28
Q

Oxygen therapy protocol

A

assessing patient’s oxygenation status

room air PaO2 is less than 60mmHg
room air SaO2 is less than 990%
acute hypoxia
intraoperative/postoperative
hypoxia suggested in sleep study
acute myocardial infarction
low cardiac output
hemoglobin less than 8.0 g/dL

→ assess PT oxygenation
—> clinical indications for therapy
—> does PT require >.40
—> appropriate high flow system
—> continuous therapy
→ increase FIO2 per guidelines

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29
Q

Aerosolized medication therapy protocol

A

agents are used to offset bronchial smooth muscle constriction

bronchospasms found
℅ dyspnea
wheezing
pulmonary hyperinflation
reduction in airflow
stridor
thick secretions
signs of increased WOB

-> PT meet indications for therapy
→ LOC
→ deep breathing
→ medications available in MDI

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30
Q

Hypoxic hypoxia (hypoxemic hypoxia)

A

= inadequate oxygen at the tissue cells caused by low arterial oxygen tension (PAO2)

hypoventilation
high altitude

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31
Q

Anemic hypoxia

A

= PAO2 is normal, but the oxygen-carrying capacity of the hemoglobin is inadequate

anemia
hemorrhage

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32
Q

Circulatory hypoxia (stagnant/hypoperfusion hypoxia)

A

= blood flow to the tissue cells is inadequate → oxygen is not adequate to meet tissue needs

slow/stagnant (pooling) peripheral blood flow arterial-venous shunts

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33
Q

Histotoxic hypoxia

A

= impaired ability of tissue cells to metabolize oxygen

cyanide poisoning

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34
Q

Anion gap

A

= Used to assess if the patient’s metabolic acidosis is caused by the accumulation of fixed acids (lactic acids, ketoacids, or salicylate intoxication) or an excessive loss of HCO3-

Equation: Anion gap= Na+ – (Cl- + HCO3-)

→ Normal range: 9 to 14 mEq/L
- Anion greater than 14 mEq/L=metabolic acidosis (elevated anion gap caused by accumulation of fixed acids in blood)

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35
Q

Oxygen consumption

A

Shows the amount of oxygen extracted by the peripheral tissues during the period of 1 minute.

Normal range= about 250ml O2/min

Formula → VO2= Qt [C(a-v) O2 x 10]

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36
Q

Work of breathing

A

= the effort that it requires to ventilate the lungs/how much energy you are expanding to expand and contract your chest

Two primary determinants of the work of breathing:
1. Lung compliance
2. Airway resistance

Formula –> Work= pressure x volume

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37
Q

P wave

A

= atrial depolarization and is Usually symmetrical and upright (0.08-0.11 sec)

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38
Q

PR interval

A

= total atrial electrical activity (0.12-0.20 sec)

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39
Q

QRS wave

A

= depolarization of the ventricle (less than .10 sec)

40
Q

ST segment

A

= time between ventricular depolarization and repolarization (less than 0.12 sec)

41
Q

T wave

A

= repolarization of ventricles
- rest, and recovery (less than .20 sec)

42
Q

U waves

A

= uncertainty possibly represent repolarization of the purkinje system
- Appears with increased regularity with PVC’s

43
Q

Pulmonary artery catheter use

A

pressure readings and waveforms are monitored to determine the catheter’s position as it moves through the right atrium (RA), right ventricle (RV), pulmonary artery (PA), and into a pulmonary capillary wedge pressure (PCWP) position

after the PCWP reading, the balloon is deflated to allow blood to flow past the tip of the catheter

44
Q

Cardiac output

A

= Cardiac output has direct influence on blood pressure

(1)= ventricular preload → degree that the myocardial fibers are stretched prior to contraction
(2)= ventricular afterload → force against which the ventricles must work to pump blood
(3)= myocardial contractility

Range= 4-8 L/min
Formula= (CO=SV x HR)

45
Q

Sputum culture test

A

= identifies the bacteria present and takes 48 to 72 hours

46
Q

Senstivity test

A

= identifies what antibiotics will kill the bacteria takes 48 to 72 hours

47
Q

Gram stain

A

= identifies whether bacteria are gram positive or gram negative takes 1 hour

48
Q

Pleural fluid

A

= the excessive fluid that accumulates between the chest cavity and lungs

useful to diagnosis and staging of the suspected or known malignancy

49
Q

Diagnostic procedures

A

= find the problem –> send off labs to figure out what the problem is –> treat the problem

50
Q

Therapeutic procedures

A

= treating the problem

51
Q

Viral/Bacteria infection differences

A

Bacteria are single cells that can survive on their own, inside or outside the body

Viruses cause infections by entering and multiplying inside the host’s healthy cells

Antibiotic medicines kill or keep many bacteria from growing but don’t treat viruses

  • Antiviral medicines help the body clear out some viruses
52
Q

Hypercapnic therapy

A

= Greater than normal amount of carbon dioxide in the blood resulting in acidosis

53
Q

Anatomic shunt

A

=exists when blood flows from right side of heart to let side without coming in contact with alveolus for gas exchange (3% cardiac output) (congestive heart disease, intrapulmonary fistula, vascular lung tumors)

54
Q

Alveolar dead space

A

= alveolus is ventilated but no perfused with pulmonary blood space is unpredictable

55
Q

Physiological dead space

A

= sum of the anatomic dead space and alveolar dead space

56
Q

SOAPIER

A

S: Subjective information

O: Objective information

A: Assessment (cause of subjective and objective data)

P: Plan (treatment selection)

I: Implementation—the actual administration ofthe specific therapy plan

E: Evaluation—collection of measurable dataregarding the effectiveness of the plan

R: Revision—any changes that may be made tothe original plan in response to the evaluation

57
Q

HIPPA

A

= Ways in which a patient’s medical files should be used or shared with others (protect)

Both the health care provider and a representative of the insurance company must explain to the patient how they plan to disclose any medical records

Patients may request copies of all their medical information and make appropriate changes to it

Patients may also ask for a history of any unusual disclosures

The patient must give formal consent should anyone want to share any health information.

The patient’s health information is to be used only for health purposes.

Without the patient’s consent, medical records cannot be used by either

When the patient’s health information is disclosed, only the minimum necessary amount of information should be released

A patient’s psychotherapy records get an extra level of protection

The patient has the right to complain to HHS about violations of HIPAA rules

58
Q

Hemodynamic measurements

A

= study of the forces that influence the circulation of blood

CVP= 0-8mmHg

RAP= 0-8mmHg

PAP= 9-18mmHg

PCWP/PAW/PAO= 4-12mmHg

CO= 4-8 L/min

59
Q

Emphysema

A

= the alveoli at the end of the smallest air passages (bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke and other irritating gasses and particulate matter

Treatment:
Low flow O2 to keep SpO2 between 88-92
Aerosolized bronchodilators
Bronchial Hygiene as indicated
Inhaled corticosteroids
Antibiotics if indicated by sputum culture
Referral to smoking cessation program, including nicotine replacement therapy
Pulmonary rehabilitation
Proper nutrition and monitor fluid intake
Consider NPPV for acute exacerbations before intubation
- Pt and Family Education

Anatomic alterations:
- Permanent enlargement and destruction of the air spaces distal to the terminal bronchioles
- Destruction of alveolar-capillary membrane
- Weakening of the distal airways, primarily the respiratory bronchioles
- Air trapping and hyperinflation

Etiology:
- Genetic predisposition
- Age and gender—COPD increases with age
- Conditions that affect normal lung growth
Exposure to particles
Socioeconomic status
Asthma/bronchial hyperreactivity
Chronic bronchitis
Respiratory infections
Tuberculosis

Chest- Xray: hyperlucency, hyperinflation, increased A-P diameter, flattened diaphragm

ABG: compensated respiratory acidosis with hypoxemia and hypercapnia

PFT: Decreased Flows (FEV1, FEV1/FVC FEF25-75%)
- estimated that between 10 and 15 million people in the United States either have chronic bronchitis, emphysema, or a combination of both

60
Q

Chronic bronchitis

A

=inflammation of the lining of the bronchial tubes, which carry air to and from the air sacs (alveoli) of the lungs. It’s characterized by daily cough and mucus (sputum) production

Anatomic alterations:
Chronic inflammation and thickening of the wall of the peripheral airways
Excessive mucous production and accumulation
Partial or total mucous plugging of the airways
Smooth muscle constriction of bronchial airways (bronchospasm)—a variable finding
Air trapping and hyperinflation of alveoli—may occur in late stages

Etiology:
Genetic predisposition
Age and gender—COPD increases with age
Conditions that affect normal lung growth
Exposure to particles
Socioeconomic status
Asthma/bronchial hyperreactivity
Chronic bronchitis
Respiratory infections
Tuberculosis

General Appearance: barrel chest, clubbing and cyanosis

Respiratory Pattern: dyspnea, accessory muscle use, pursed-lip breathing

Breath Sounds: diminished aeration with bilateral expiratory wheeze

Diagnostic Chest Percussion: tympanic or hyperresonant

Cough: congested, productive thick sputum

Chest- Xray: hyperlucency, hyperinflation, increased A-P diameter, flattened diaphragm

ABG: compensated respiratory acidosis with hypoxemia and hypercapnia

PFT= Decreased Flows (FEV1, FEV1/FVC FEF25-75%)

Treatment:
Low flow O2 to keep SpO2 between 88-92
Aerosolized bronchodilators
Bronchial Hygiene as indicated
Inhaled corticosteroids
Antibiotics if indicated by sputum culture
Referral to smoking cessation program, including nicotine replacement therapy
Pulmonary rehabilitation
Proper nutrition and monitor fluid intake
Consider NPPV for acute exacerbations before intubation
Pt and Family Education

61
Q

Bronchiectasis

A

= Chronic dilation and distortion of one or more bronchi as a results of excessive inflammation and destruction of bronchial walls, blood vessels, elastic tissue and smooth muscle. This results in impaired mucociliary clearance causing accumulation of copious amounts of bronchial secretions

Causes of bronchiectasis are commonly classified as:
Acquired bronchial obstruction
Congenital anatomic defects
Immunodeficiency states
Abnormal secretion clearance
Miscellaneous disorders (e.g., alpha1-antitrypsin deficiency)

Chest X-ray: hyperlucent lung fields, depressed or flattened flattened diaphragm, enlarged or elongated heart.

ABG: Mild to moderate cases :acute alveolar hyperventilation with hypoxemia
- Severe cases: chronic ventilatory Failure with hypoxemia

PFT: decreased flows, severe cases may also have decreased volumes

Bronchogram or CT: dilated bronchi, increased bronchial wall opacity

Patient Assessment
History of pulmonary infections
General appearance: cyanosis, barrel chest, clubbing\
Respiratory Pattern: tachypnea, dyspnea, accessory muscle use, pursed-lip breathing.

BS: wheezing, diminished breath sounds

Diagnostic percussion: hyperresonat or tympanic notes

Cough: productive of purulent, foul-smelling secretions, hemoptysis, sputum will separate into 3-layers

Increased hematocrit and hemoglobin

Elevated white blood count if acutely elevated

Sputum examination
Streptococcus pneumoniae
Haemophilus influenzae
Pseudomonas aeruginosa
Anaerobic organisms

General treatment plan:
The treatment of the underlying disease may not possible
Oxygen therapy
Bronchopulmonary hygiene to Controlling airway secretions and obstruction
– CPT. C&D

Lung expansion therapy

Surgical resection of involved portions if necessary

Controlling pulmonary infections- Preventing complications

Antibiotics, bronchodilators, and expectorants, Vaccinations

62
Q

Alpha1-antitrypsin

A

= made in the live and its job is to protect the lungs from neutrophil elastase which if left uncontrolled breaks down connective tissue

Ranges= 150-350 mg/dL
- Genetically have MM alpha1-antitrypsin phenotype

Low serum concentration= ZZ alpha 1- antitrypsin

Heterozygous= MZ alpha1-antitrypsin
- cigarette smoking increases risk

63
Q

Asthma

A

= A chronic, inflammatory, obstructive, non-contagious airway disease with varying levels of severity, characterized by exacerbations of wheezing and coughing

Etiology:
Obesity
Many factors have been linked to an increased risk of developing asthma, although it is often difficult to find a single, direct cause.
Sex (The male sex is a risk factor for asthma in children)
Infections
Exercise-induced asthma
Outdoor/Indoor air pollution
Drugs, food additives, and food preservatives
Extrinsic asthma (Allergic or Atopic asthma)
Asthma episodes clearly linked to the exposure of a specific allergen (antigen):
House dust
Mites
Furred animal dander
Cockroach allergen
Fungi
Molds
Yeast
Occupational sensitizers (Occupational Asthma)

Intrinsic asthma (Nonallergic or Nonatopic asthma)
Asthma episode cannot be directly linked to a specific antigen or extrinsic factor.
Onset usually occurs after the age of 40 years
Drugs
Food additives and preservatives
Exercise-induced bronchoconstriction
Gastroesophageal reflux
Sleep (nocturnal asthma)
Emotional stress
Perimenstrual asthma (catamenial asthma)
Allergic bronchopulmonary aspergillosis

Anatomic Alterations of the Lungs
Smooth muscle constriction of bronchial airways (bronchospasm)
Excessive production of thick, whitish bronchial secretions
Mucous plugging
Hyperinflation of alveoli (air trapping)
In severe cases, atelectasis caused by mucous plugging
Bronchial wall inflammation leading to fibrosis (in severe cases, caused by remodeling)

Patient Assessment-History and Physical exam
SOB-pursed-lip breathing, chest tightness
Appearance of the chest –increased A-P diameter during an attack
Respiratory Pattern- Accessory muscle usage, retractions (more so in kids)
Diagnostic Chest Percussion – hyperresonant/tympanic note
BS - Diffuse wheezing, bilateral wheezing, diminished breath sounds, prolonged expiration
Physical Appearance – diaphoresis
Vitals – tachycardia, tachypnea
Decreased blood pressure during inspiration
Increased blood pressure during expiration
eczema
hay fever
family history of asthma
atopic diseases

Chest X-ray –During an attack increased A-P diameter, translucent lung fields, depressed or flattened diaphragm

ABG – Initially acute respiratory alkalosis with hypoxemia then acute respiratory acidosis

PFT –Spirometry shows reduced flowrates during an attack

Post-bronchodilator: if asthma return to normal

Significant response if FEV1 increases at least 12% and 200ml (Peak Flow Meter)

Bronchial Provocation test –FEV1 decreases significantly when methacholine is given

Other Diagnostics for Asthma
Allergy testing
Exhaled nitric Oxide
Exercise-induced bronchoconstriction (EIB)

Abnormal Laboratory Tests and Procedures
Eosinophilia
Charcot-Leyden crystals
Casts of mucus from small airways (Kirschman spirals)
IgE level (elevated in extrinsic asthma)

Long-term goals for asthma management are:
Symptom control
Risk reduction of future exacerbations

Control-based asthma management program
Controller medications
Reliever (rescue) medications
Add-on therapies for patients with severe asthma

Stepwise management approach
STEP 1—As-needed Reliever Inhaler
STEP 2—Low Dose Controller Medication Plus Needed Reliever Medication
STEP 3—One or Two Controllers, Plus As-needed Reliever Medication
STEP 4—One or Two Controller Plus As-needed Reliever Medication
STEP 5—Higher Level Care and/or Add-on Treatment

Management of an Asthma Attack
Oxygen Therapy
Aerosol Therapy
Corticosteroids
Close monitorin
Intubation and mechanical ventilation if vent failure or respiratory arrest occurs

Adjunct therapies
Heliox therapy
Magnesium sulfate
Subcutaneous epinephrine

Long Term Control of Asthma
Asthma triggers should be eliminated, minimized, or avoided to prevent acute attacks
Control medications: LABA, ICS, mast cell stabilizers, leukotriene inhibitors
Asthma Action plan based on peak flow monitoring.

Refer pt to specialist if
Difficulty confirming diagnosis
Suspected occupational asthma
Risk of asthma death (example prior intubation due to asthma)
Evidence or risk of significant treatment side effects (drug interactions, allergic reactions)

64
Q

Atelectasis

A

= abnormal condition of the lungs characterized by the partial or total collapse of previously expanded alveoli

Etiology:
cystic fibrosis, lung tumors, chest injuries, fluid in the lung and respiratory weakness
You may develop atelectasis if you breathe in a foreign object.
Pneumothorax is one of several causes of atelectasis
Obesity
Operative and postoperative supine position
Advanced age
Use of inadequate tidal volume during mechanical ventilation
Malnutrition
Free fluid in the abdominal cavity
Presence of a restrictive lung disorder

Anatomic:
Alveoli of primary lobules (microatelectasis or subsegmental atelectasis)—very common
Lung segment—fairly common
Lung lobe—less common
Entire lung—rare

Diagnosis:
Physical Exam

Chest X-ray: Provides pictures of the chest to help identify areas of collapsed lung tissue (GOLD Standard)

Computed tomography (CT) scan: Creates detailed images of the lungs and chest cavity to help determine the cause of atelectasis

Bronchoscopy: A thin, flexible tube with a camera is inserted into the windpipe to detect and remove blockages

Vital signs: Increased Respiratory rate (tachypnea), Heart rate (pulse), Blood pressure
- Cyanosis

Chest assessment findings:
Increased tactile and vocal fremitus
Dull percussion note
Bronchial breath sounds
Diminished breath sounds

When atelectasis is caused by mucous plugs:
Crackles
Whispered pectoriloquy

*PFT – Restrictive Findings

Prevention:
Precipitating factors for postoperative atelectasis should be identified
High-risk patients should be monitored closely
Preventive measures should be prescribed for high-risk patients
Incentive spirometry
Perform breathing exercises and get up and move around as soon as you can after surgery or extended periods of bed rest

Treatment:
Oxygen therapy protocol
Airway clearance therapy protocol
Lung expansion therapy protocol
- IS
- IPPB
- CPAP
- PEEP

Mechanical ventilation protocol

65
Q

Pneumonia

A

= An infectious inflammatory process that primarily affects the gas exchange area of the lungs causing capillary fluid to pour into the alveoli. This process leads to inflammation of the alveoli, alveolar consolidation and atelectasis.
- viruses account for 50% pneumonia

Anatomic alterations:
Inflammation of the alveoli
Alveolar consolidation
Atelectasis (e.g., aspiration pneumonia)

Etiology:
Extremely Common
Causes include bacteria, viruses and aspiration
Bacteria, viruses, fungi, protozoa, parasites, tuberculosis, anaerobic organisms, aspiration, and the inhalation of irritating chemicals such as chlorine

General appearance: Diaphoretic, cyanotic

Respiratory Pattern: Tachypnea

BS: Crackles, bronchial, whispered pectoriloquy

Diagnostic Chest Percussion: Flat or dull note over consolidation

Cough Productive: yellow/green sputum, may also be rust color

Vitals: Fever, (bacteria >100° F and viral < 101° F) increased HR, RR and BP

Chest X-ray- Increased density in area of consolidation and atelectasis, air bronchograms possible pleural effusion

ABG-Acute alveolar hyperventilation with hypoxemia

PFT: decreased volumes and capacities

CBC: Increased WBC with bacterial infection, decreased with viral

Culture and Sensitivity to determine cause

Treatment:
Oxygen therapy
Bronchial hygiene
Hyperinflation
Mechanical ventilation for those in respiratory failure
VAP- protocol for those intubated
Antibiotics as indicated from sputum culture and sensitivity
Thoracentesis if pleural effusion present
Bedrest
Adequate fluid intake
OTC meds to reduce fever, aches, pain and control cough

66
Q

Turberculosis

A

= A contagious chronic bacterial infection that primarily affects the lungs

TB pathogen, Mycobacterium tuberculosis—a rod-shaped bacterium with a waxy capsule
It may involve almost any part of the body

Classified as either:
Primary TB- Follows the patient’s first exposure to the TB pathogen
Reactivation TB- reappearance of TB months or even years after the initial infection has been controlled
Disseminated TB- infection from TB bacilli that escape from a tubercle and travel to other sites throughout the body by means of the bloodstream or lymphatic system

Anatomic:
Alveolar consolidation
Alveolar-capillary destruction
Caseous tubercles or granulomas
Cavity formation
Fibrosis and secondary calcification of the lung parenchyma
Distortion and dilation of the bronchi
Increased bronchial airway secretions

Diagnosis:
Mantoux tuberculin skin test
Acid-fast bacilli (AFB) sputum cultures
The QuantiFERON-TB Gold (QFT-G) test
The rapid Xpert MTB/RI assay

Treatment:
Pharmacologic agents
Consists of 2 to 4 drugs for 6 to 9 months
Isoniazid (INH) and rifampin (Rifadin) are first-line agents prescribed for the entire 9 months
Isoniazid is considered to be the most effective first-line antituberculosis agent
Rifampin is bactericidal and is most commonly used with isoniazid
When the TB is resistant to one or more of these agents, at least three or more antibiotics must be added to the treatment regimen and the duration should be extended

Treatment:
Oxygen therapy protocol
Airway clearance therapy protocol
Mechanical ventilation protocol
Infectious control measures protocols

67
Q

Fungal diseases

A

Histoplasmosis (Histoplasma capsulatum)= Most common fungal disease in the United States

Prevalence is especially high along the major river valleys of the Midwest
Birds themselves do not carry the organism, although the H. capsulatum spore may be carried by bats

Fungal culture—considered the gold standard for detecting histoplasmosis
Fungal stain
A positive test result is 100% accurate

Serology- A relatively fast and accurate test

Coccidioidomycosis= Caused by inhalation of the spores of Coccidioides immitis
Endemic in hot, dry regions
Especially prevalent in California, Arizona, Nevada, New Mexico, Texas, and Utah
“California fever,” “Desert rheumatism,” “San Joaquin Valley Disease,” and “Valley Fever”

Screening and diagnosis
Made by direct visualization of distinctive spherules in microscopy of the patient’s sputum, tissue exudates, biopsies, or spinal fluid

Blastomycosis (Blastomyces dermatitidis)
Chicago disease, Gilchrist’s disease, American blastomycosis
Occurs in people living in the South-Central and Midwestern United States and Canada

Primary portal of entry is the lungs
Cough is frequently productive, and the sputum is purulent

Screening and diagnosis—Blastomycosis
Direct visualization of yeast in sputum smears
Culture of the fungus
opportunistic pathogens (Candida albicans, Thrush, Cryptococcus neoformans)
The high nitrogen content of pigeon droppings

Aspergillus= Found in soil, vegetation, leaf detritus, food, and compost heaps

Anatomic

Alveolar consolidation

Alveolar-capillary destruction

Caseous tubercles or granulomas

Cavity formation

Fibrosis and secondary calcification of the lung parenchyma

68
Q

Lung abscess

A

= (also known as “necrotizing pneumonia” or “lung gangrene”) is characterized as a localized air-and fluid-filled cavity, which is collection of purulent exudate that is composed of liquefied white blood cell remains, proteins, and tissue debris. The air-and fluid-filled cavity is encapsulated in a so-called pyogenic membrane that consists of a layer of fibrin, inflammatory cells, and granulation tissue.

Major pathologic or structural changes
Alveolar consolidation
Alveolar-capillary and bronchial wall destruction
Tissue necrosis
Cavity formation
Fibrosis and calcification of the lung parenchyma
Bronchopleural fistulae and empyema
Atelectasis
Excessive airway secretions

Thoracentesis
Color
Odor
RBC count
Protein
Glucose
Lactic dehydrogenase (LDH)
Amylase
pH
Wright’s, Gram, and acid fast bacillus (AFB) stains
Aerobic, anaerobic,tuberculosis, and fungal cultures
Cytology

69
Q

Sepsis

A

= Extreme response to an infection, Infection can occur in lungs, GI tract,urinary tract, nasal sinuses, surgical sites ext.

Etiology:
Immunosuppressed patients, especially those with cancer or HIV
Patients taking steroids and anti-rejection drugs
Very young babies
The elderly (co-morbidities)

General appearance: Chills, diaphoretic, nausea and vomiting

Respiratory pattern: Tachypnea and dyspnea

BS: Crackles and rhonchi

Percussion: flat or dull over area with consolidation

Cough Productive of yellow/green sputum

Vitals: increased RR, HR, decreased BP and fever

Chest x-ray: Increased density if atelectasis or consolidation is present (PNA) otherwise can be normal

ABG: if pulmonary involvement can be abnormal

CBC: Increased WBC

Blood cultures: Need to be done to determine cause

Sputum: C&S if lung involvement

Treatment:
Support Circulation and perfusion
IV hydration (Monitor IO)
Antimicrobial therapy based on cultures
Standard precautions to prevent spread (could be higher if cause indicates

70
Q

Shunt equation

A

Shunt equation→ Qs= CcO2 - CaO2

           —--------------------

Qr= CcO2 - CvO2

1.PAO2= (PB- PH2O) FIO2 - PaCO2 (1.25)

2.CcO2= (Hb x 1.34) + (PAO2 x 0.003)

3.CaO2= (Hb x 1.34 x SaO2) + (PaO2 x 0.003)

4.CVO2= (Hb x 1.34 x SVO2) + (PVO2 x 0.003)

Qs= CcO2 - CaO2

——————-—-

Qr= CcO2 - CvO2

71
Q

Tidal volume (vT)

A

MALE→ 500mL & FEMALE→ 400-500mL
= the volume of air that moves into and out of the lungs in one quiet breath

72
Q

Inspiratory reserve volume (IRV)

A

MALE→ 3100mL & FEMALE→1900mL
= the maximum volume of air that can be inhaled after anormal tidal volume inhalation

73
Q

Expiratory reserve volume (ERV)

A

MALE→ 1200mL & FEMALE→ 800mL
= the maximum volume of air that can be exhaled after anormal tidal volume exhalation

74
Q

Residual volume (RV)

A

MALE→ 1200mL & FEMALE→ 1000mL
= The remaining amount of air in the lung after maximal exhalation (Boyle’s law to measure)

75
Q

Vital capacity (VC)

A

= the maximum amount of air that can be exhaled after maximal inspiration (IRV+VT+ERV)

76
Q

Inspiratory capacity (IC)

A

=the volume of air that can be inhaled after normal exhalation (VT + IRV)

77
Q

Functional residual capacity (FRC)

A

= the volume of air remaining in the lungs after normal exhalation (ERV + RV)

78
Q

Total lung capactiy

A

= the maximum amount of air the lungs can accommodate (IC + FRC)

79
Q

Residual volume/total lung capacity ratio (RV/TLC x 100)

A

= The percentage of TLC occupied by the residual volume (NO GAS EXCHANGE CAN OCCUR)

80
Q

What is normal alveolar ventilation in a healthy lung and what is the formula used to determine alveolar ventilation?

A

= DefiIs the inspired air that reaches the alveoli is effective in terms of gas exchange

Alveolar ventilation= (tidal volume – dead space) x breaths/min
→ (500-150) x 12 =4200 ml/min

81
Q

What is the normal range for the CVP? What if the CVP is high or low what does this mean?

A

= Pressure within the superior vena cava, which reflects the pressure under which the blood is returned to the right atrium

  • Normal range= 2-6 mmHg or 4-12 cm water

High= respiratory issues or Pulmonary disease fluid overload

Increase CHF → no change —> COPD: increase → Lung collapse: increase → Hypovolemia: decrease → Pulmonary embolism: increase

Low CVP: low blood volume

82
Q

What is the normal range for the PCWP? What if the PCWP is high or low what does this mean?

A

= Left ventricular filling, represent left atrial pressure, and assess mitral valve function.

*Normal range= 2-6 mmHg or 4-12 cm water

High PCWP= increase after load

Low PCWP= decrease after load

Con pulmonale: decrease → CHF: increase → COPD: no change → Lung collapse: decrease → Hypovolemia: decrease → Pulmonary embolism: decrease

83
Q

What is the normal range for the mean pulmonary artery pressure? What do high and low numbers mean

A

Normal range= 9-18mmHG

Con Pulmonale: decrease → CHF: increase → COPD: increase → Lung collapse: increase → Hypovolemia: decrease → Pulmonary Embolism: Increase

84
Q

The inflation reflex depends upon stimulation of which type of receptor?

A
  1. stimulate ALPHA RECEPTORS (pulmonary vascular system CONSTRICT)
  2. stimulate BETA2 receptors (relax airway)
85
Q

What is the FRC if the Vt is 500 mL, RV 1000 mL, and ERV 1200 mL? Draw the Volume Box

A

ERV 1200ml + RV 1000ml= 2200FRCml

86
Q

Phase 0 of the action potential?

A

= ventricular muscle fibers are activated between 60-100 times/min by electrical impulses by sinoatrial (SA) node (produces rapid stroke/rapid inflow of sodium)
- (voltage inside cell at the end= 30+mV)

87
Q

Phase 1 of action potential

A

=Initial repolarization- channels for K+ open and permit K+ flow out of cell –> action produces early (downward stroke) (incomplete) repolarization (downward stroke)

88
Q

Phase 2 action potential

A

= Plateau state- =slow inward Ca2+ –> slows outward flow of K+ (prolongs contraction of myocardial cells)

89
Q

Phase 3 action potential

A

= Final rapid repolarization- inward flow of Ca2+ stops –> outward flow of K+ accelerated (rate of repolarization accelerates)

90
Q

Phase 4 action potential

A

= Resting or polarized state- excess Na+ inside cell & loss ofK+ return to normal ion pumps –> additional Na+/Ca2+ pump remove excess Ca2+ from cell (voltage sensitive ion channels return to pre-depolarized permeability)

91
Q

Explain water vapor pressure

A

Water in gaseous form (47 torr)
- can exist as liquid, gas, or solid

92
Q

P50

A

= Represents the partial pressure at which hemoglobin is 50% saturated with oxygen when there are 2 oxygen molecules on each hemoglobin molecule (P50 = 27 torr)

93
Q

Oxyhemoglobin dissociation curve shifts RIGHT → P50 INCREASES

A

low pH (more acidotic)= curves right

increase in body temp = curves right

PCO2 increase = curves right

2,3 BPG increase = curves right

94
Q

Oxyhemoglobin dissociation curve shifts LEFT → P50 DECREASES

A

high pH = curves left

decrease in body temp = curves left

PCO2 decrease = shift left

Fetal hemoglobin = shifts left

Carbon monoxide hemoglobin = shifts left

95
Q

Explain the respiratory exchange ratio

A

Ratio of amount of oxygen that moves into pulmonary capillary blood to amount of carbon dioxide that moves out of pulmonary blood into alveoli (1.25 factor)

96
Q

Define the respiratory quotient and what is normal?

A

= Gas exchange between the system capillaries and the cell is called internal respiration. Under normal circumstances about 250ml of oxygen are consumed by the tissues during 1 min –> in exchange the cells produce about 200ml carbon dioxide

  • Clinically the ratio between the volumes of oxygen consumed (VO2) is called the respiratory quotient(RQ)

Vo 250ML O2/min = 0.8 (normal)

RCP (8 decks)

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