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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Restrictive lung disease
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 
26
Bronchopulmonary Hygiene therapy protocol
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 
27
Lung expansion protocol
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  
28
Oxygen therapy protocol
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
29
Aerosolized medication therapy protocol
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
30
Hypoxic hypoxia (hypoxemic hypoxia)
= inadequate oxygen at the tissue cells caused by low arterial oxygen tension (PAO2) hypoventilation  high altitude 
31
Anemic hypoxia
= PAO2 is normal, but the oxygen-carrying capacity of the hemoglobin is inadequate  anemia hemorrhage
32
Circulatory hypoxia (stagnant/hypoperfusion hypoxia)
= 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 
33
Histotoxic hypoxia
= impaired ability of tissue cells to metabolize oxygen  cyanide poisoning 
34
Anion gap
= 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) 
35
Oxygen consumption
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]
36
Work of breathing
= 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 
37
P wave
= atrial depolarization and is Usually symmetrical and upright (0.08-0.11 sec)
38
PR interval
= total atrial electrical activity (0.12-0.20 sec)
39
QRS wave
= depolarization of the ventricle (less than .10 sec)
40
ST segment
 = time between ventricular depolarization and repolarization (less than 0.12 sec)
41
T wave
= repolarization of ventricles - rest, and recovery (less than .20 sec)
42
U waves
= uncertainty possibly represent repolarization of the purkinje system - Appears with increased regularity with PVC’s 
43
Pulmonary artery catheter use
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
Cardiac output
= 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
Sputum culture test
= identifies the bacteria present and takes 48 to 72 hours
46
Senstivity test
= identifies what antibiotics will kill the bacteria takes 48 to 72 hours
47
Gram stain
= identifies whether bacteria are gram positive or gram negative takes 1 hour
48
Pleural fluid
= the excessive fluid that accumulates between the chest cavity and lungs  useful to diagnosis and staging of the suspected or known malignancy 
49
Diagnostic procedures
= find the problem --> send off labs to figure out what the problem is --> treat the problem
50
Therapeutic procedures
= treating the problem 
51
Viral/Bacteria infection differences
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
Hypercapnic therapy
= Greater than normal amount of carbon dioxide in the blood resulting in acidosis 
53
Anatomic shunt
= 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
Alveolar dead space
 = alveolus is ventilated but no perfused with pulmonary blood space is unpredictable 
55
Physiological dead space
= sum of the anatomic dead space and alveolar dead space 
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SOAPIER
S: Subjective information O: Objective information A: Assessment (cause of subjective and objective data) P: Plan (treatment selection) I: Implementation—the actual administration of the specific therapy plan E: Evaluation—collection of measurable data regarding the effectiveness of the plan R: Revision—any changes that may be made to the original plan in response to the evaluation
57
HIPPA
= 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
Hemodynamic measurements
= 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
Emphysema
= 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
Chronic bronchitis
= 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
Bronchiectasis
= 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
Alpha1-antitrypsin
= 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
Asthma
= 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)
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Atelectasis
= 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
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Pneumonia
= 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
Turberculosis
= 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
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Fungal diseases
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
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Lung abscess
= (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
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Sepsis
= 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
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Shunt equation
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
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Tidal volume (vT)
MALE→ 500mL & FEMALE→ 400-500mL = the volume of air that moves into and out of the lungs in one quiet breath
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Inspiratory reserve volume (IRV)
MALE→ 3100mL & FEMALE→1900mL = the maximum volume of air that can be inhaled after a normal tidal volume inhalation
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Expiratory reserve volume (ERV)
MALE→ 1200mL & FEMALE→ 800mL = the maximum volume of air that can be exhaled after a normal tidal volume exhalation
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Residual volume (RV)
MALE→ 1200mL & FEMALE→ 1000mL = The remaining amount of air in the lung after maximal exhalation (Boyle’s law to measure)
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Vital capacity (VC)
= the maximum amount of air that can be exhaled after maximal inspiration (IRV+VT+ERV)
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Inspiratory capacity (IC)
= the volume of air that can be inhaled after normal exhalation (VT + IRV)
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Functional residual capacity (FRC)
= the volume of air remaining in the lungs after normal exhalation (ERV + RV)
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Total lung capactiy
= the maximum amount of air the lungs can accommodate (IC + FRC)
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Residual volume/total lung capacity ratio (RV/TLC x 100)
= The percentage of TLC occupied by the residual volume (NO GAS EXCHANGE CAN OCCUR)
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What is normal alveolar ventilation in a healthy lung and what is the formula used to determine alveolar ventilation? 
= 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
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What is the normal range for the CVP? What if the CVP is high or low what does this mean? 
= 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
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What is the normal range for the PCWP? What if the PCWP is high or low what does this mean?  
= 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
What is the normal range for the mean pulmonary artery pressure? What do high and low numbers mean 
Normal range= 9-18mmHG Con Pulmonale: decrease → CHF: increase → COPD: increase → Lung collapse: increase → Hypovolemia: decrease → Pulmonary Embolism: Increase
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The inflation reflex depends upon stimulation of which type of receptor? 
1. stimulate ALPHA RECEPTORS (pulmonary vascular system CONSTRICT) 2. stimulate BETA2 receptors (relax airway)
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What is the FRC if the Vt is 500 mL, RV 1000 mL, and ERV 1200 mL? Draw the Volume Box 
ERV 1200ml + RV 1000ml= 2200FRCml
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Phase 0 of the action potential? 
= 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)
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Phase 1 of action potential
= Initial repolarization- channels for K+ open and permit K+ flow out of cell --> action produces early (downward stroke) (incomplete) repolarization (downward stroke)
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Phase 2 action potential
= Plateau state- =slow inward Ca2+ --> slows outward flow of K+ (prolongs contraction of myocardial cells)
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Phase 3 action potential
= Final rapid repolarization- inward flow of Ca2+ stops --> outward flow of K+ accelerated (rate of repolarization accelerates)
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Phase 4 action potential
= 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) 
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Explain water vapor pressure
Water in gaseous form (47 torr)  - can exist as liquid, gas, or solid
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P50
= 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)
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Oxyhemoglobin dissociation curve shifts RIGHT → P50 INCREASES
low pH (more acidotic)= curves right  increase in body temp = curves right PCO2 increase = curves right  2,3 BPG increase = curves right 
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Oxyhemoglobin dissociation curve shifts LEFT → P50 DECREASES
high pH = curves left decrease in body temp = curves left PCO2 decrease = shift left Fetal hemoglobin = shifts left Carbon monoxide hemoglobin = shifts left 
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Explain the respiratory exchange ratio
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)
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Define the respiratory quotient and what is normal? 
= 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) RQ= Vco2 = 200ML Co2/min --------------------------------------------           Vo        250ML O2/min = 0.8 (normal)