mechanisms pulmonary

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How many primary bronchii does trachea branch into?: 2 primary that branch into several smaller ones
at which branches to bronchii become bronchioles: 12th-16th branches
where do the terminal bronchioles occur: 17th-24th branches
What is found at the end of the terminal bronchioles?: alveolar ducts, sacs, and alveoli
What happens when bronchioles 12-16 over secret mucous or constrict?: asthma or chronic bronchitis
Where is the "dead space"?: down to the 16th branch
Dead space=: 150 mL of air per breath that's not being exchanged; remains in the passageways
where does diffusion of O2 take place?: from terminal bronchii to the alveoli
approx how many alveoli?: 300 million
what's the total surface area?: 50-90 sq. meters
Acinus=: everything distal to the terminal bronchioles
What happens to the acinus in emphysema?: they lose their alveolar sacs and gas diffusion area decreases
How do the bronchii contract to increase airway resistance?: via smooth muscle cells that wrap around the bronchs. and contract to narrow the airway
How do the alveoli receive blood?: pulmonary arterioles divide into small capillaries that run in sheets btw./among alveoli
Which muscles are used for inspiration?: -diaphragm
-external intercostals
-accessory inspiratory muscles (scalenes and sternocleidomastoid)
Which are oriented like levers btw. the ribs and cause elevation of the ribcage?: external intercostals
which of these is innervated by the phrenic nerve (from C4)?: diaphragm
Which are used during very labored breathing and also turn the head?: accessory inspiratory muscles (scalenes and sternocleidomastoid)
Which pulls on the sternum and middle third of the clavicle?: sternocleidomastoid
Which hooks onto ribs 1 & 2: scalenes
Where does sternocleidomastoid originate?: mastoid of skull
What is the scalenes innervated by?: cervical plexus (c1-c4)
Which muscle separates thoracic from the abdominal cavity?: diaphragm
Where does scalenes originate?: from the transverse process of cervical region
where is the chest tube inserted in a thoracostomy?: superiorly on the rib (can cut nerve or vein if underneath)
what's a pneumothorax?: fluid in the pleural space
What are the expiratory muscles?: -diaphragm
-abdominal muscles
-internal intercostals
what do the abdominal muscles do?: pull lower ribs down
What is the action of the diaphram in expiration: relaxation
What do the internal intercostals do?: pull down ribs and compress the thorax
What does a spirometer measure?: static lung volumes- how much air is blown
What are the static lung volumes?: -TV
-IRV
-ERV
-RV
-FRC
-VC
Resting Tidal Volume (TV)=: -the amount of air inhaled/exhaled when breathing normally
-about 500mL
Inspiratory Reserve Volume (IRV)=: -the amount of air that can be taken in, in addition to a normal breath
Expiratory Reserve Volume (ERV)=: -amt of air that can be expelled after inhaling all the way
-about 1000mL
Residual Volume (RV)=: -amt of air left in the lungs after expelling as much air as possible
-1000mL
Functional Residual Capacity (FRC)=: =ERV + RV
Vital Capacity =: -the max amt. of air that can be moved
= IRV+TV+ERV
What do the static lung volumes tell about lungs and chest wall?: reflect their elastic properties
Why do pt's have difficulty getting air out in obstructive diseases?: due to lost collagen and elastin, narrowed passages, and excess mucous secretions
What happens to the small and terminal bronchioles?: they collapse
What static lung volume is an indicator?: a dec'd FVC (longer than 6 secs)
Is slow VC okay in obstructive?: yes
what are examples of obstructive diseases?: emphysema, asthma, chronic bronchitis
Why do pt's have diff breathing in restrictive lung diseases: due to lost elasticity
what happens to the lungs: they become fibrosed- like a tough non-compliant football
What happens to the VC?: it's smaller
where is the visceral pleura located: on the lung
where is parietal pleura located: on the inside of the chest cavity
what lies between these two layers: fluid
what is this space called: interpleural space
what does the space allow for: causes the lungs to stick to the inside of the chest wall- creates a strong bond
is it positive or negative pressure: negative pressure b/c the chest wall wants to go out and the lungs want to recoil back inward
(a fluid vacuum)
What causes lung recoil: surface tension
At FRC, how expanded is the chest: 60%
Surface tension=: a collection of molecular forces that occurs whereever gas/fluid interface exists
what causes it: the thin fluid layer between the alveolar cells and the air
Surfactant=: fluid which decreases surface tension to keep lungs from collapsing
chemical name for surfactant: Dipalmitolecithin
what produces it: type 2 epithelial cells within the alveoli
Law of LaPlace=: P= 2(T/r) pressure= 2*(tension/radius)
how does this apply to pressure in the lungs?: -pressure in a fluid bubble is a fx of the surface tension of the fluid and the radius of the bubble
-if 2 bubbles (alveoli) have diff diameter but are lined by fluids w/ the same surface tension, the pressure (resistance) inside the smaller bubble will be greater, so smaller alveoli are more diff to fill with air than lg. ones
How does surfactant solve this problem?: -its more concentrated in smaller alveoli, making their surface tension less than the larger ones
-this lower tension helps equalize pressure so smaller ones can inflate
-they receive a proportionate amt of air as large ones
Lung compliance=: change in volume/change in pressure
what shape is the compliance curve: sigmoid
what's on the x-axis: intrapleural pressure (Pip)
whats on the y axis: lung volume
Where does a change in Pip produce the biggest change in volume: middle (less at beginning and end)
what is the "equilibrium" pt. btw recoil and chest wall expansion?: FRC
where does most of normal insipirated air go to in the lungs: the base
where does most output of the right ventricle go: the alveolar capillaries in base of lung
When can mismatches in the ventilation/perfusion (V/Q) ratio occur?: -mucus plug blocks ventilation
-pulmonary embolism blocks blood flow
What does the pulmonary funtion test, FEV1 test: forced expiratory volume at one second
whats normal FEV1 value?: 75% of FVC
How much CO goes to pulmonary (alveolar)vasculature for oxygenation: 99%
where does the rest go?: bronchiole vasculature and doesnt get oxygenated
what happens to it?: from the thoracic aorta there is a separtate ciculation that oxygenates the lung parenchyma and gets pumped back into pulmonary veins and mixes w/ oxygenated blood to by pumped from LV
why is Hgb never 100% saturated: b/c some supplied the lungs and was deoxygenated
Mean Arterial Pressure=: Pd +(Ps-Pd)/3; normal is 93mmHg; P in RA is 0
What is LV CO?: 5L/min; RV=LV CO normally
Is pulmonary vascular resistance higher or lower compared to rest of body: lower- if it goes up, blood backs up and RV can fail
What division of the nervous system controls how much blood goes to the lung: ANS, including parasympathetic and sympathetic
Hypoxia=: area of lung that's not well ventilated (= degree of ventilation)
what does the degree of hypoxia determine: -status of the pulmonary arterioles (dilated or constricted)
-i.e. a decr in ventilation causes arterioles to constrict and that area shuts down
-vasoconstriction is directly proportional to hypoxia
does skeletal muscle work like this: no-its the opposite- less flow means dilation
what does pulmonary vasoconstriction help to maintain: V/Q ratio
what happens with chronic hypoxia: -local arterioles continuosly vasoconstricted
-total pulmonary vascular resistance inc's
-RV failure
who does sleep apnea most affect: overweight males
whats the most important control of pulmonary vascular resistance: hypoxia
besides hypoxia what else causes inc's pulmonary vascular resistance: -pulmonary embolism
-fibrosis
-LV failure
what are causes of fibrosis: -systemic sclerosis
-scleroderma
-sarcoidosis
-coal miners lung
-silicosis
-black lung
how does LV failure cause RV failure: it cant pump out what the RV feeds in so its pumping against more resistance
Which receptors are the controllers of air flow: muscarinic and beta
where are muscarinic located: smaller bronchi and bronchioles
sympathetic or parasympathetic?: adrenergic sympathetic fibers
how?: fibers send APs to receptor that releases NE to dilate (not all receptors are innervated)
when does it occur: when we're in a vegetative state
where are betas located: on bronchioles, arterioles, heart muscle, and the GI tract
what do asthma meds like proventil do?: -acts as a B2 agonist- binds and dilates
-can also bind B1 receptors in heart to inc heart rate
Where are respiratory rhythm generators (RRGs) located: in the medulla
what are the 2 types: -dorsal respiratory grp
-ventral respiratory grp
which controls inspiratory phase: dorsal
what does ventral control: expiration and inspiration
how are primary RRGs modified: from the pons
what are the abnormal respiratory rhythms?: 1. Bradypnea (slow)
2. Tachypnea(fast)
3. Cheyne-Strokes (waxy and wany ventilatory depth w/ periods of apnea)
4. Hyperventilation (rate of vent exceeds tissue demand resulting in hypocapnia)
5. Hypoventilation (rate of vent is less than tissue demand resulting in hypercapnia)
6. Hyperpnea (inc'd ventilation due to inc'd O2 demand from tissues)
What controls rate and depth of NL respiration?: 1. Stretch receptors
2. Irritant receptors
3. J (Juxta capillary) receptors
4. Cerebral Cortex
5. Limbic System
6. Pain
Which allows voluntary control over breating/respiration?: Cerebral cortex
Which increases rate and depth?: pain
Which are found in smooth muscle of bronchioles?: stretch receptors
what do they do: creat autonomic endpoint to inhalation
Which are found in lung parenchyma btw. alveoli?: J receptors
what do they do?: detect interstitial distortions from pulmonary distortions (i.e. edema/fibrosis cause rapid and shallow breathing)
which are found in epithelial layers of airways?: irritant
what do they detect?: anything noisesome thats inhaled (stops breathing- then causes rapid shallow breathing)
Which controls breathing based on emotion?: limbic - our "emotional brain"
what are the three "f's" that are controlled by the limbic?: feeding, fighting, fornication
What are the controllers of long term respiration?: Chemoreceptors- Peripheral and Central
What are the 3 peripheral chemoreceptors?: 1. Carotid Sinus
2. Carotid Bodies
3. Aortic Bodies
Which has the highest rate of blood flow in the whole body?: Carotid sinus
Where are carotid bodies found?: on medial side of carotid sinus
what are they innervated by?: by carotid sinus nerve which joins glossopharyngeal nerve to enter brainsteam
Where are aortic bodies located?: aortic arch
What innervates aortic bodies?: afferent vagus fibers
What do both aortic and carotid bodies do?: -monitor plamsa for O2 content (hypoxia monitoring)
-report to RRGs in medulla
which are more important: carotid
what do they do if stimulated by hypoxia?: cause an increase in the ventilation and/or depth of respiration
Where are central chemoreceptors located?: on the ventrolateral portion of the medulla
whats the only thing they respond to?: changes in the plasma pCO2 b/c the blood brain barrier in medulla prevents entrance of any molecules with charge (CO2 is neutral and small)
Which receptors are responsible for 80% of regulation of plasma pCO2: central chemos (other 20% is carotid bodies)
Which respond faster to plasma pCO2 changes: carotid chemos
Which are used for long term?: central chemos
Whats the pH2O at 37 degrees C?: 47mmHg
Whats the pO2 of inhaled air: 713 mmHg
Whats the pO2 in lower bronchiole tree: 150 mmHg (100 mmHg in alveoli)
pO2 of arterial blood=: 100mmHg
pCO2 of arterial blood=: 40mmHg
pO2 of venous blood=: 40
pCO2 of venous blood=: 46
2 ways of carriage of O2:: 1. physical solution-O2 is dissolved in plasma
2. bound to Hgb
How much O2 does plasma carry?: 0.3mL O2/dL plasma
How much O2 does Hgb carry?: 15mL O2/dL blood
3 ways of carriage of CO2:: 1. physical solution (in plasma)
2. form of carbamino compounds
3. carried as bicarbonates
How much CO2 does plasma carry?: 2.76mL CO2/dL plasma
How does CO2 form carbamino compounds?: combines with N2 group of amino acid, occurs in plasma proteins and in Hb
What's the most common way CO2 is carried?: as bicarbonate- 70% exhaled CO2 has been carried as bicarbonate
Is more CO2 or O2 carried in physical solution (plasma)?: CO2
Bohr Effect=: inc. in blood pCO2 in the tissues causes a dec in Hb affinity for O2
-allows O2 to be released to tissues
Haldane Effect=: inc in blood pO2 in lungs causes a dec in Hb affinity for CO2
-allows CO2 to let go
at what pressure is Hb 50% saturated: 26mmHg
what is p50?: plasma O2 at which Hb is 50% saturated
what causes the oxy-Hb dissociation curve to shift to the right?: -dec in pH
-inc. in pCO2
-inc. in temp
-inc. 2.3DPG (Hb releases O2 more)
what does a shift to the right mean?: -p50 is increased
-dec'd affinity of Hb for O2
-shifts b/c to keep Hb 50% saturated, it must encounter higher pO2
-present during exercise
what causes the oxy-Hb dissociation curve to shift left?: -inc'd pH
-dec pCO2
-dec temp
-dec 2.3DPG
what does a shift to the left mean?: -p50 is decreased
-inc'd affinity for Hb for O2
-shifts b/c to keep Hb 50% saturated, it must encounter lower pO2
-present in vegetative state
What does the diffusing capacity of the lungs measure (DLco): ability of lung tissue to allow diffusion at the right level
Which problems are due to bronchi and bronchiole constriction?: 1. asthma
2. acute/chronic bronchitis
3. bronchiecstasis
4. bronchogenic cancer
what problems are due to histological areas of the lung (alveoli)?: 1. atelectasis
2. pneumothorax
3. air space diseases (pnemonia and emphysema)
What are diseases of the plurea?: 1. pleural effusion
2. pneumothorax
what diseases result from problems with the vessels?: 1. pulmonary embolism
2. primary pulmonary HTN
3. CHF
What are the problems with interstitium btw. alveoli?: 1. infection (pneumonia)
2. Fibrosis (restrictive, idiopathic, environment, autoimmune)
At what rate is peural fluid normally formed on the parietal pleural surface?: about 0.1 ml/kg/hr
The aqueous phase of this fluid is reabsorbed by the___________: the visceral pleural capillaries
The protein phase is reabsorbed by ____________: the parietal pleural lymphatics
Balance between fluid formation and reabsorption normally leaves how much in the pleural space: 5 -15 ml (not dectable on cxr)
what is a pleural effusion: an abnormal accumulation of fluid and is often detectable on plain chest film
5 major types of pleural effusion:: 1. exudate
2. transudate
3. empyema
4. hemothorax
5. chylothorax
An exudate has at least one of these features:: - more than Â½ the protein content of the same patientâ€™s serum

- more than 6/10 the lactate dehydrogenase (LDH) content of the same patientâ€™s serum

- an LDH content greater than 2/3 the upper limit of â€œnormal serumâ€
are exudates active or passive: they're active abnormal cellular process
causes of exudates:: 1. Infections: TB, fungus/parasite, pneumonia (bacterial or viral)
2. Cancer
3. PE
4. uremia
5. drug reaction
which are the 2 most common causes of exudates: cancer and pneumonia
What is a transudate?: the passive movement of fluid resulting from:
1. increased vascular hydrotstatic pressure
2. decreased plasma oncotic pressure
3. increased negative intrapleural pressure
What are the 4 causes of transudate?: 1. CHF
2. Nephrotic Syndrome
3. Constrictive Pericarditis
4. Acute Atelectasis
which of these is the most common cause of pleural effusion overall: CHF
how does CHF cause pleural effusion?: LV failure causes pressure to increase in the pulmonary vessels ----->
increased hydrostatic pressure
which causes decreased plasma oncotic pressure?: nephrotic syndrome
what happens with constrictive pericarditis?: noncompliant pericardium restricts ventricular filling and mimics CHF
how does acute atelectasis cause transudate?: increases negative intrapleural pressure
how does a PE cause transudate?: it leads to incâ€™d Pul.Vasc. Resistance thus incâ€™d hydro-static pressure which leads to transudate
what is an empyema?: a form of exudate where fluid is turbid or purulent due to infection in the pleural space itself
Whats a hemothorax?: gross blood in pleural space sually due to chest trauma
Whats a chylothorax?: milky in appearance due to presence of cholesterol complexes
when is chylothorax most common?: in tuberculous pleuritis or rheumatoid
sn/sx of small Pleural effusion (less than 200mL):: assymptomatic (no physical findings)
sn/sx of large Pleural effusion (more than 200mL):: -dyspnea
-lung compression
- dullness to percussion
- massive effusion on one side may push the trachea (and therefore the tracheal
air column ) to the opposite side.
what does pleuritic chest pain indicate?: exudative pleural effusion
what does pleural friction rub indicate?: pleurisy
X-ray findings for pleural effusion:: -blunting of the costophrenic sulcus
-â€œThickeningâ€ of interlobal and/or interlobular lung fissures on plain film
-Loculated fluid
-Crescentic line or meniscus
What causes thickening: due to fluid which has invaded the space by capillary action and shows up
on Xray as a white line
What is loculated fluid: fluid trapped by pleural adhesions in one area along the chest wall
what does this look like on film?: a white shadow with its broad base toward the chest wall and a point toward the lung
What causes the crescentic line or meniscus?: if effusion doesn't go to apex, upper edge of opacification is curved
When is a thoracentesis performed?: when etiology of effusion is in doubt, esp if exudate is suspected
thoracentesis=: aspiration of some of the fluid with a syringe and needle by inserting it through an intercostal space which the Xray shows to be somewhere below the upper level of the effusion
- must also be placed immediately above the rib in order to avoid hitting intercostal nerves and vessels which lie immediately below any rib
Tx for exudative:: Tube thoracostomy- chest tube
where is the chest tube placed: low in the chest in order to get most of the fluid above it, typically in the 5th or 6th interspace at the midaxillary line or more posterior
what is a chief goal of drainage?: prevent the progression from exudative to fibropurulent and more â€œorganizedâ€ stages in which a â€œpeelâ€ may be formed which can trap a portion of the lung and cause permanent loss of lung function
Tx for transudative:: -first try tx for underlying condition
-if the effusion is large enough to compress the lung and affect breathing or cause tracheal/mediastinal shift, then a chest tube is placed for drainage
Tx for hemothorax:: -chest tubes
-thoracotomy for large volumes or clots
Thoracotomy =: surgical procedure which leaves the patient with a pneumothorax, for which a thoracostomy tube must then be placed
what is a pulmonary embolus?: anything which moves from somewhere in the systemic venous circulation to the right heart and becomes ejected by the right ventricle into the pulmonary circulation
what is the most common cause of pulmonary embolism?: a thrombus that forms in the deep veins of the leg (a DVT), dislodges to become an embolus and goes to the lungs (also called a a pulmonary thromboembolus)
Other causes of pulm. embs?: 1. Air embolus: during neurosurgery, or from central venous catheter
2. Amniotic fluid embolus: during active labor
3. Fat embolus: from long bone or hip fractures
4. Foreign body embolus: a piece of an I.V. catheter
5. Tumor cell embolus: renal cell carcinoma
Essentials of Dx:: -abrupt onset of dyspnea, tachypnea, chest pain, hemoptysis and/or syncope
-high risk for venous thrombosis (DVT)
-Unmatched or mismatched defects on V/Q scan
-Diagnostic findings on pulmonary angiogram or spiral CT
what inc's risk of a DVT?: 1. Non-ambulation: the bedridden patient or long distance traveler
2. Recent surgery: ie total hip replacement
3. Woman on oral contraceptives who smokes
4. Obesity
5. Cancer,esp adenocarcinoma of breast, pancreas, prostate, ovary
6. Hereditary Hypercoagulability
7. prolonged dehydration
what are the risk factors for pulm emb?: same as DVT
Most common veins for emboli to arise from:: Deep veins of the calf:
-Anterior & posterior tibial veins
- Peroneal vein
Do they form in superficial veins (i.e. small or great saphenous)?: No
Where can a thrombus propagate or dislodge to from the deep veins of the calf?: Popliteal vein and Ileofemoral vein to form a proximal DVT
What are the sn/sx of a DVT?: -FEW OR NO SX
- dull ache or tightness in leg, esp. while walking
- distention of superficial collateral veins, slight edema maybe
-Homan's sn = leg pain on passive dorsiflexion at ankle
Why is dx difficult?: -Dx only by history and physical
-Sns & sx of PE are not specific for PE
-sn/sx aren't conclusive
Sn/sx of PE:: -dyspnea and pain on inspiration
-tachypnea >16
-tachycardia
-Cough, wheezing, crackles, hemoptysis, leg pain all possible
-Pleural friction rub, cyanosis possible
-Accentuated pulmonary component of second heart sound ( S2
-Homan's sn
Lab findings:: 1. CXR (to rule out pneumonia, pneumothorax, massive pleural effusion, TB, or preexisting CHF)
2. ABG's: show hypoxemia, and usually respiratory alkalosis due to hyperventilation
3. ECG: may show sinus tachycardia and non-specific ST segment and T wave changes
On ECG, a Tall R wave in V1 indicates:: acute right heart strain from sudden increase in pulmonary vascular resistance
ECG will help rule out:: AMI
Why does a PE cause RV failure?: A clot blocks a major flow artery so there are fewer flow channels for the blood. This inc's pulmonary vascular resistance and RV can't adjust to work harder.
Which test is used to determine the presence of a thrombus ANYWHERE:: Plasma D-dimer level: Lack of increased D-dimer is strong evidence for no thrombus
What is used to detect a DVT?: 1. Contrast Venography (will show intraluminal filling defect in vein- not as common as other 2)
2. Duplex ultrasound with color flow doppler
3. GADOLINIUM-ENHANCED magnetic resonance venography
To detect a PE?: 1. Spiral CT
2. Pulmonary angiography (done after a V/Q)
3. V/Q Scan
In a V/Q scan which is done first?: Q- perfusion tested via radiocontrast injection.
NL shows 2 whole lung silhouettes
What will the Q scan show if there's a thrombus?: A perfusion defect:
a hole in the picture, where blood is not flowing
Usually, no perfusion defect=: No PE
If a perfusion defect is found, then what?: do a V scan
V-scan =: patient inhales radioactive gas and a camera takes a ventilation picture. If there is no parenchymal pathology in the lungs, they show up again as two whole lung silhouettes
Does a PE causing matching V and Q defects (i.e. same part of lung shows up defective)?: no- mismatching defect
why?: b/c a thrombus of a PE is in pulmonary artery /arteriole, not in the bronchi / bronchioles
What other pathology shows V/Q defects?: emphysema shows matching defects
If you find 2 or more unmatched Q defects:: PE V. LIKELY
If you find mismatched Q and V defects:: PE LIKELY
If you find matched Q and V defects:: PE UNLIKELY (suspect emphysema)
If V/Q is equivocal but PE suspicion is high, order a:: pulmonary arteriogram
Prevention (the best Tx):: -avoid risk factors for DVT
-after surgery, early ambulation, intermittent pneumatic compression stockings, and low dose heparin or Low Molecular Weight Heparin ( LMWH)
What are exs. of low molecular wt. heparin drugs?: -Lovenox ( enoxaparin)
-Innohep (tinzaparin)
Tx of confirmed PE:: -Immediate anticoagulation with unfractionated Heparin
-or LMWH may be used
-Longterm 3 - 6mos anticoagulation with Coumadin (warfarin)
What are the 4 main categories of a pneumothorax?: 1. primary spontaneous
2. secondary spontaneous
3. traumatic
4. tension
Which occurs as a complication of lung disease?: secondary
Which occurs in the absence of underlying lung disease?: primary
Which is due to blunt or penatrating trauma or iatrogenic causes?: traumatic
What are iatrogenic causes?: -subclavian or internal jugular vein catheterization
- thoracentesis
- percutaneous lung biopsy
- pleural biopsy
- pulmonary barotrauma from mechanical overventilation
What happens in a tension PTX?: air enters thorax during inspiration but does not exit on expiration
- positive interpleural pressure > ambient pressure
Causes:: trauma, CPR or mechanical ventilation
What are sn of any PTX?: -Acute onset ipsilateral chest pain (minimal to severe)
-Dyspnea
What are the objective findings?: Mild cases-minimal -if PTX < 15% of hemithoraxâ€¦perhaps only mild tachycardia

Severe cases- unilateral chest expansion, tracheal & mediastinal shift toward side
opposite PTX, breath sounds & fremitus decreased or absent, percussion hyperresonance or tympany, CXR shows â€œvisceral-pleural lineâ€ and/or area of thorax with markedly absent pulmonary vasculature (no lung there)
Who does primary PTX mostly affect?: tall, thin boys or young men, 10-30 yo; smoking inc's risk
Cause?: rupture of subpleural apical blebs due to high negative pleural pressure
What is secondary PTX associated with?: other lung diseases: pneumonia, TB, Cystic fibrosis, Asthma, COPD
What is Catamenial PTX (a secondary type) associated with?: onset of menses +/- 3-5 days and also intrathoracic endometriosis
What is an important contemporary cause of PTX on mechanical ventilation: Pulmonary barotrauma

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