Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
69 Cards in this Set
- Front
- Back
|
Define acute resp failure:
|
hypoxemic state where pao2<50, pco2>50, pH<7.25.
|
|
|
Differentiate between hypoxemic and hypercapnic resp failure (causes):
|
Hypercapnic is caused by inadequate ventilation (rate/vol). Hypoxic is caused by poor gas exchange (shunt).
|
|
|
What are the causes of pulm edema?
|
1. elevated PCWP
2. decreased plasma onc pressure 3. increased pulm vasc permeability. |
|
|
At what PCWP does pulm edema set in?
|
Usually PCWP>20 causes pulm edema, but it can occur at lower wedges if the capillary oncotic pressure is low (dec hgb or albumin).
|
|
|
What are causes of increased alveocapillary permeability?
|
ARDS, toxic gases, sepsis.
|
|
|
Define compression atelectasis:
|
caused by the external pressure exerted by a tumor, fluid, or air in the pleural space or by an abdominal distention pressing on a portion of the lung, causing the alveoli to collapse.
|
|
|
What is absorption atelectasis?
|
It results from removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen or anesthetic agents (decreased distending pressure of the gas). Example: FIO2>60% leads to "nitrogen washout". O2 has lower partial pressure than nitrogen and cannot exert enough pressure to keep alveoli inflated, leading to collapse.
|
|
|
What is bronchiectasis?
|
Abnormal persistant dilation of the bronchi. May be related to repeated untreated respiratory infections.
|
|
|
What is bronchiolitis?
|
An inflammatory obstruction of the small airways or bronchioles. Usually diffuse. Leads to dec. V/Q and hypoxemia and hypercapnia.
|
|
|
What is an open pneumothorax?
|
Air gets sucked into the pleural space during inspiration and expired during expiration. Can be r/t external trauma (eg. stabbing) or internal visceral pleura rupture.
|
|
|
What is a tension pneumothorax?
|
Similar to open pneumothorax except that the site of rupture acts as a one-way valve allowing air into the pleural space but then trapping it. The pressure then builds and compresses the lung, mediastinum and other lung. Is immediately life threatening.
|
|
|
What is spontaneous pneumothorax?
|
Occurs unexpectedly in otherwise healthy individuals, usually tall thin men. Usually r/t emphasematous bleb rupture. May develop tension pneumo.
|
|
|
What is a pleural effusion?
|
Fluid collection in the pleural space. Can lead to compression atelectasis.
|
|
|
What types of conditions could cause a transudative pleural effusion?
|
Caused by CHF (elevated wedge), or conditions that cause decreased plasma oncotic pressure. It is mostly water.
|
|
|
What is an empyema? What could cause it?
|
It is pus in the pleural space. Most common with pneumonia. Lymphatics become blocked spilling contaminated lymph fluid into pleural space.
|
|
|
What is an exudative pleural effusion? What could cause this?
|
Less watery,has high concentrations of white blood cells and plasma proteins. Occurs in response to infection or inflammation where increased capillary permeability leads to effusion.
|
|
|
What is pleurisy and what might cause it?
|
It is inflammation of the pleura. Often preceeded by an upper respiratory infection.
|
|
|
What is pulmonary fibrosis and what could cause it?
|
Can be caused by healing (scar tissue) formation after ARDS or TB or anything that damaged the alveocap membrane. Or can be from inhalation of harmful substances like coal dust or asbestos. May be ideopatithic.
|
|
|
What changes in the lung would you expect from pulmonary fibrosis?
|
Decreased lung compliance, dec. diffusing capacity of the alveolocapillary membrane leads to hypoxia. Poor prognosis.
|
|
|
What is flail chest?
|
Multiple sequential rib fractures lead to paradoxic movement of the chest with breathing. Can cause impaired gas movement in/out of lung. Must be stabilized until healed.
|
|
|
What is oxygen toxicity?
|
Fio2 levels of greater than 50% for greater than 24H can lead to damage to alveocap membranes, disruption of surfactant production, interstitial and alveolar edema and decreased compliance. It is caused by O2 free radical damage.
|
|
|
What is pneumoconiosis?
|
Lung changes r/t inhalation of inorganic dust particles, usually in the workplace, often after years of exposure. Silica, asbesots, and coal are the most common causes. Dust deposits are permanant and can lead to pulm fibrosis. "Black Lung Disease" is a form of this.
|
|
|
Describe the process of ARDS:
|
Acute injury leads to inflammation of the alveo-cap membrane and causes severe pulmonary edema. (This is non-cardiogenic pulmonary edema).
|
|
|
What is the effects of inflammatory mediators in ARDS?
|
They cause increased capillary permeability and pulm edema. They also cause pulm vasoconstrition (deadspace), and elevated PA pressures. Can also lead to SIRS and MODS for similar reasons.
|
|
|
Describe the progressive effects of ARDS:
|
Alveolar endothelium damage injurs type2 alveolar cell and decreases surfactant production. This causes alveolar collapse and leads to decreased compliance. Over days, the lungs fibrose and leads to severe shunting.
**Doug: why don't you remember SURFACTANT!! |
|
|
What are the 2 hallmark signs of ARDS? (per the text)
|
1. non-cardiogenic pulmonary edema (patchy bilat infiltrates) 2. refractory hypoxemia
|
|
|
What are some of the changes that may occur in postoperative respiratory failure? What might cause this?
|
atelectasis, pneumonia, pulm edema, and pulm emboli. They cause decreased compliance, VQ mismatch. May be caused by intraop hypotension and/or sepsis.
|
|
|
What is the hallmark sign and symptom of obstructive pulmonary disease?
|
Dyspnea and wheeze.
|
|
|
What effect would obstructive pulmonary disorders have on FVC, FEV1 and FEV1/FVC?
|
FVC might me normal or low.
FEV1 will be reduced due to blocking of expired air (air trapping). FEV1/FVC will be reduced in porportion to the amount of airway obstruction. Elevated FRC and RV (air trapping) occurs later. |
|
|
Define asthma:
|
Chronic bronchial inflammation leading to wheezing, chest tightness, bronchospasm and cough. Reversible airway obstruction.
|
|
|
Is asthma genetic or environmentally linked?
|
Both probably. There appears to be a genetic link, yet environment triggers may lead to exacerbation of symptoms.
|
|
|
How is does asthma classification work?
|
Four stages(levels) based on severity of SYMPTOMS regardless of cause. Stage 4 is the worst.
|
|
|
How do pao2 and pco2 vary over the course of a severe asthma attack in patients?
|
Initially, respiratory alkalosis is manifest r/t hyperventilation. As airways constrict, air trapping leads to impaired gas exchange and pao2 drops and pco2 rises. Rising pco2 is a critical warning sign that respiratory FAILURE is imminent.
|
|
|
True or False: clinical assessment can reasonably assess degree of airway obstruction in asthma pts.
|
False. Assessment often underestimates the level of obstruction. It is best to use peak flow measurements (baseline vs during attack) and a blood gas.
|
|
|
What is status asthmaticus?
|
Severe bronchospasm refractory to standard treatments. May be life threatening as patient fatigues and succumbs to respiratory failure.
|
|
|
What is COPD?
|
Pathologic lung changes consistent with emphysema or chronic bronchitis. Abnormal expiratory airflow refractory to pharmacologic intervention.
|
|
|
How is chronic bronchitis defined/diagnosed?
|
hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year (usually winter) for 2 consecutive years. Common in smokers
|
|
|
What chronic changes occur in chronic bronchitis?
|
Increased number and size of mucous glands and goblet cells in airway epithelium. This causes very thick mucous and impaired ciliary function. Infection only makes mucous and inflammation worse. Air trapping occurs leading to R to L shunting and hypoxemia and hypercapnia.
|
|
|
What are the long term sequelae of chronic bronchitis?
|
Marked hypoxemia leads to polycythemia and cyanosis. Hypoxic/hypercapnic vasoconstriction can even result in pulm htn, cor pulmonale and death. V/Q mismatching (shunt) can result in hypercapnia.
|
|
|
What changes in PFTs would support a diagnosis of chronic bronchitis?
|
Decreased FEV1, eventually significantly reduced FVC and FEV1. Later, elevated FRC and RV (air trapping).
|
|
|
True or False: the physical effects of damage caused by chronic bronchitis can be reversed if the pt gets treatment.
|
False. The *progression* can be slowed/stopped but damage done is irreversible.
|
|
|
Describe what air trapping means:
|
It describes how air can easily enter the alveoli but, due to airway constriction or mucous, can't escape (becomes trapped). This can cause hyperinflation changes of the alveoli. Remember, this *increases surface tension and *decreases lung compliance(due to effect of surfactant reversing LaPlace's Law).
|
|
|
In COPD, what are the long term effects on O2/CO2 balance in the body? Why?
|
COPDers become chronic CO2 retainers and chronically hypoxic. The elevated CO2 desensitizes the central chemoreceptors in the brain stem to changes in pH and respiratory drive in response to CO2 changes is greatly diminished. Ventilation changes then occur when the less-sensitive carotid and aortic chemoreceptors sense a drop in paO2. That's why you don't want to put your COPDer pt on a NRB mask !
|
|
|
What is emphysema?
|
abnormal permanent enlargement of acini and alveolar descruction WITHOUT fibrosis. Is caused by elastic lung tissue destruction NOT inflammation.
|
|
|
What is the pathophysiological cause of emphysema?
|
Primary emphysema: inherited deficiency of alpha1-antitrypsin (an antielastase) which prevents the breakdown of elastin in the lung.
Secondary emph: same as primary except deficiency is caused by exposure to inhaled toxins. |
|
|
What are bullae and blebs?
|
Bullae are the hyperinflated alveoli in COPD and blebs are air spaces adjacent to the pleura (can blow-out and cause pneumothorax).
|
|
|
What are some clinical findings common to pts with emphysema?
|
DOE, minimal or no sputum production, pt is thin, tachypneic with prolonged expiration, accessory muscle use, increased A/P chest dimension.
|
|
|
What are PFT findings that support a diagnosis of emphysema?
|
Decreased FVC and FEV1. Increased FRC, RV and TLC. TLC may be doubled! Decreased diffusing capacity due to alveocap mem destruction.
|
|
|
What are the long term complications of emphysema?
|
Prolonged disease process, infections, cor pulmonale, death.
|
|
|
What are the two types of emphysema?
(structurally not primary vs secondary) |
Centriacinar emphysema: septal destruction occurs in the resp bronchiles and alveolar ducts, usually in the upper lobes of the lung. The alveolar sack remains intact. (most common with smokers and chronic bronchitis).
Panacinar emphysema: involves the entire acinus with more diffuse involvement including the lower lung. Common with elderly and alpha1-antitrypsin deficiency. |
|
|
What is pneumonia?
|
Infection of the lower respiratory tract.
|
|
|
What is the most common cause of CAP?
|
Strep Pneumoniae. Low mortality rate.
|
|
|
What is a common cause of pneumonia in dormatories and barracks?
|
Mycoplasma pneumoniae.
|
|
|
What is the most common cause of viral CAP?
|
influenza.
|
|
|
What are the main organisms that cause nosocomial pneumonia (HAP)?
|
pseudomonas aeruginosa and staph aureus.
|
|
|
What is the type of pneumonia common in pts with HIV/AIDS?
|
pneumocystis carinii. But mycobacteria and fungi are also common due to depressed immune function.
|
|
|
What is the most common route of infection leading to pneumonia?
|
Aspiration.
|
|
|
Bronchitis and PE not discussed on these slides. Review on your own.
|
OK?
|
|
|
What is pulmonary HTN?
|
an elevation of pulm artery pressure of 5 to 10 mmHg (normal 15-18).
|
|
|
What are the two type of pulm htn?
|
primary and secondary. primary is ideopathic, secondary is related to factors that exogenously elevate PA pressures (CHF, hypercapnic or hypoxic pulm vasoconstriction, PE).
|
|
|
What is the major adverse development of untreated pulm htn?
|
cor pulmonale.
|
|
|
What is the treatment for secondary pulm htn?
|
remove the underlying cause.
|
|
|
What is the most common specific site of laryngeal cancer?
|
The true vocal cords (glottis).
|
|
|
What is the key symptom of laryngeal cancer?
|
Progressive worsening hoarseness.
|
|
|
What are statistical odds of getting non-SCLC vs SCLC?
|
75% are non-small cell.
25% are small cell. |
|
|
Briefly describe Squamous cell carcinoma:
|
30% of lung cancers. Usually located near the hilus and project into bronchi. Do not metastasize until late. Surgical removal prior to metastasis is best treatment.
|
|
|
Briefly describe Adenocarcinoma:
|
40% of lung cancers. Arises from glandular tissue in lung. Usually small, <4cm, and peripheral. Often found on routine CXR. Early mets leads to low survival rate even with surgical removal.
|
|
|
Describe Large Cell Carcinoma:
|
10% of lung cancers. Is totally undifferentiated. Diagnosed by exclusion. Generally are peripheral but can be central and can affect tracheal position. Surgical therapy limited if mets develop. Radiation and chemo not much help.
|
|
|
Describe small cell carcinoma and what is a common unusual finding with this disease:
|
20% of lung cancers. Worst prognosis due to rapid growth and early/wide mets. Untreated will kill in 1-3 mos. Commonly develops paraneoplastic syndromes (SIADH most common). Usually advanced at time of DX due to symptoms being common with smoking SX.
|
