RCP 103 midterm Flashcards
Peripheral chemoreceptors
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
Hypoxemia
caused by DECREASED v/q ratio, pulmonary shunting, venous admixture
Central chemoreceptors
DRG/VRG are responsible for coordination of respiration stimulation by H+ ions in the CSF
Deflation reflex
compressed/deflated lungs (atelectasis)= INCREASED RR
Hering-Breuer
when receptors are stretched (during deep inspiration) reflex response is triggered to decreased the ventilatory rate
- does NOT occur when temperature is LOW
Irritation reflex
when the lungs are exposed to irritants, compressed, deflated irritant receptors are stimulated
- RR, cough, bronchospams INCREASE
Juxtapulmonary-capillary receptors (J receptors)
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
Reflex from cartoid/aortic snius baroreceptors
activation causes DECREASED HR, RR –> INCREASED systemic blood pressure
INCREASED HR, RR –> DECREASED systemic blood pressure
Autonomic Nervous System
Regulates involuntary functions (heart rate, smooth muscle, and glands)
Sympathetic NS
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)
Parasympathetic NS
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
Respiratory zone
- type 1 cells for STRUCTURE
- type 2 cells (PRODUCE SURFACTANT)
FVC
= maximum volume of gas that can be exhaled as forcefully and rapidly as possible after a maximal inspiration
FEV1/FEV ratio
= comparison of the amount of air exhaled in 1 second to the total amount exhaled during the FVC maneuver
FVC, FEV1, FEV1/FEV ratio
= 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
Respiratory Failure
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
Hyperventilation
- 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
Superimposed
- 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
Normal ABGs
pH= 7.35-7.45
PaCO2= 35-45
PaO2= 80-100
HCO3-= 22-28
Respiratory Alkalosis
pain
hypoxia
anxiety
pH= high
PaCO2= low
HCO3-= normal
Metabolic alkalosis
diuretics
pH= high
PaCO2= normal
HCO3-= high
Metabolic acids
diabetes
kidney condition
pH= low
PaCO2= normal
HCO3-= low
Compensated
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
Obstructive lung disease
INCREASE airway resistance (Raw) → INCREASE time constant= asthma, chronic bronchitis, emphysema, cystic fibrosis
RV, Vt, FRC increased
VC, IC, IRV, ERV decreased
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
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
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
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
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
Hypoxic hypoxia (hypoxemic hypoxia)
= inadequate oxygen at the tissue cells caused by low arterial oxygen tension (PAO2)
hypoventilation
high altitude
Anemic hypoxia
= PAO2 is normal, but the oxygen-carrying capacity of the hemoglobin is inadequate
anemia
hemorrhage
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
Histotoxic hypoxia
= impaired ability of tissue cells to metabolize oxygen
cyanide poisoning
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)
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]
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
P wave
= atrial depolarization and is Usually symmetrical and upright (0.08-0.11 sec)
PR interval
= total atrial electrical activity (0.12-0.20 sec)
QRS wave
= depolarization of the ventricle (less than .10 sec)
ST segment
= time between ventricular depolarization and repolarization (less than 0.12 sec)
T wave
= repolarization of ventricles
- rest, and recovery (less than .20 sec)
U waves
= uncertainty possibly represent repolarization of the purkinje system
- Appears with increased regularity with PVC’s
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
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)
Sputum culture test
= identifies the bacteria present and takes 48 to 72 hours
Senstivity test
= identifies what antibiotics will kill the bacteria takes 48 to 72 hours
Gram stain
= identifies whether bacteria are gram positive or gram negative takes 1 hour
Pleural fluid
= the excessive fluid that accumulates between the chest cavity and lungs
useful to diagnosis and staging of the suspected or known malignancy
Diagnostic procedures
= find the problem –> send off labs to figure out what the problem is –> treat the problem
Therapeutic procedures
= treating the problem
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
Hypercapnic therapy
= Greater than normal amount of carbon dioxide in the blood resulting in acidosis
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)
Alveolar dead space
= alveolus is ventilated but no perfused with pulmonary blood space is unpredictable
Physiological dead space
= sum of the anatomic dead space and alveolar dead space
SOAPIER
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
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
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
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
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
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
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
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)
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
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
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
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
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
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
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
Tidal volume (vT)
MALE→ 500mL & FEMALE→ 400-500mL
= the volume of air that moves into and out of the lungs in one quiet breath
Inspiratory reserve volume (IRV)
MALE→ 3100mL & FEMALE→1900mL
= the maximum volume of air that can be inhaled after anormal tidal volume inhalation
Expiratory reserve volume (ERV)
MALE→ 1200mL & FEMALE→ 800mL
= the maximum volume of air that can be exhaled after anormal tidal volume exhalation
Residual volume (RV)
MALE→ 1200mL & FEMALE→ 1000mL
= The remaining amount of air in the lung after maximal exhalation (Boyle’s law to measure)
Vital capacity (VC)
= the maximum amount of air that can be exhaled after maximal inspiration (IRV+VT+ERV)
Inspiratory capacity (IC)
=the volume of air that can be inhaled after normal exhalation (VT + IRV)
Functional residual capacity (FRC)
= the volume of air remaining in the lungs after normal exhalation (ERV + RV)
Total lung capactiy
= the maximum amount of air the lungs can accommodate (IC + FRC)
Residual volume/total lung capacity ratio (RV/TLC x 100)
= The percentage of TLC occupied by the residual volume (NO GAS EXCHANGE CAN OCCUR)
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
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
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
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
The inflation reflex depends upon stimulation of which type of receptor?
- stimulate ALPHA RECEPTORS (pulmonary vascular system CONSTRICT)
- stimulate BETA2 receptors (relax airway)
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
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)
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)
Phase 2 action potential
= Plateau state- =slow inward Ca2+ –> slows outward flow of K+ (prolongs contraction of myocardial cells)
Phase 3 action potential
= Final rapid repolarization- inward flow of Ca2+ stops –> outward flow of K+ accelerated (rate of repolarization accelerates)
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)
Explain water vapor pressure
Water in gaseous form (47 torr)
- can exist as liquid, gas, or solid
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)
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
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
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)
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)
Vo 250ML O2/min = 0.8 (normal)
