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601 Cards in this Set

  • Front
  • Back
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
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?
-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)?
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?
Which hooks onto ribs 1 & 2
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?
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?
-abdominal muscles
-internal intercostals
what do the abdominal muscles do?
pull lower ribs down
What is the action of the diaphram in expiration
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?
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
Functional Residual Capacity (FRC)=
Vital Capacity =
-the max amt. of air that can be moved
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?
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
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
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
fluid which decreases surface tension to keep lungs from collapsing
chemical name for surfactant
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
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?
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
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
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
besides hypoxia what else causes inc's pulmonary vascular resistance
-pulmonary embolism
-LV failure
what are causes of fibrosis
-systemic sclerosis
-coal miners lung
-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?
cholinergic parasympathetic innervations
Ach binds causing constriction and bronchiole lumen narrows
when does it occur
when we're in a vegetative state
where are betas located
on bronchioles, arterioles, heart muscle, and the GI tract
sympathetic or parasympathetic?
adrenergic sympathetic fibers
fibers send APs to receptor that releases NE to dilate (not all receptors are innervated)
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
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?
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?
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
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?
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=
pCO2 of arterial blood=
pO2 of venous blood=
pCO2 of venous blood=
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)?
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
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 ½ the protein content of the same patient’s serum

- more than 6/10 the lactate dehydrogenase (LDH) content of the same patient’s serum

- an LDH content greater than 2/3 the upper limit of “normal serum”
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
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 inc’d Pul.Vasc. Resistance thus inc’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):
-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?
X-ray findings for pleural effusion:
-blunting of the costophrenic sulcus
-“Thickening” 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
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 “organized” stages in which a “peel” 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)?
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?
- 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
-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:
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=
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
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:
If you find mismatched Q and V defects:
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's a pneumothorax?
separation of the visceral and parietal pleurae by a volume of air, leading to a collapse under the surface tension-induced recoil of its collective alveoli
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?
Which occurs in the absence of underlying lung disease?
Which is due to blunt or penatrating trauma or iatrogenic causes?
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
trauma, CPR or mechanical ventilation
What are sn of any PTX?
-Acute onset ipsilateral chest pain (minimal to severe)
What are the objective findings?
Mild cases-minimal -if PTX < 15% of hemithorax…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 “visceral-pleural line” 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
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
Who is this most often seen with
ARDS patients requiring high positive inspiratory pressure or PEEP
Suspect TENSION PTX if:
-severe dyspnea/marked tachycardia
-tracheal or mediastinal shift
-systemic hypotension ( due to decreased venous return )
-widespread percussion hyperresonance or tympany
What do labs show for PTX?
- ABGs show hypoxemia (low plasma pO2) & acute repiratory alkalosis from hyperventilation in most pts.
What does a CXR show?
- visceral pleural line = definitive diagnosis (may see only on expiratory film)
-may see pleural effusion, i.e blunting of costophrenic angle (sulcus)
-may see shift of tracheal air column toward a NL PTX
-may see shift of tracheal air column & mediastinum away from a tension PTX.
pneumonia, AMI, PE
What are possible complications of PTX?
-subcutaneous emphysema (air in subcutaneous tissue)
-pneumomediastinum on CXR: suspect rupture of esophagus or bronchus as cause of PTX
What constitutes a small PTX?
< 15% of hemithorax
Tx for small PTX?
-observation (often resolves)
-O2 suppl. (may increase rate of air reabsorption)
-Aspiration with 16g angiocath)
-Serial CXRs to follow progress
What constitutes a lg PTX?
>15% of hemithorax
Tx for large?
-admit to hospital
-stop smoking (or 50% reoccurance)
-average recurrence after spontaneous PTX = 30%
What are characteristics of restrictive lung disease?
decreased lung compliance, which translates into increased inspiratory effort and smaller static and dynamic lung volumes
What are the 2 main categories of RLD?
Extrapulmonary causes and parenchymal (interstitial)diseases
What are extrapulmonary causes?
anything that causes chest wall deformities (limiting inspiration):
-muscular dystrophy
-obesity hypoventilation syndrome
What are the 5 parenchymal (interstitial) diseases?
1. Primary Pulmonary Disease (Idiopathic pulmonary fibrosis)
2. Systemic Disease
3. Environmental and Occupational
4. Infections (fungal, PCP, or virus)
5. Drug Induced
What are the systemic causes?
1. hyaline membrane disease (kids)
3. Autoimmune diseases (rheumatoid, SLE, systemic sclerosis, dermato/polymyositis
4. Pulmonary edema & pulmonary venous
What are the environmenta/occupational causes?
1. Pneumonconioses (inorganic dusts; i.e. asbestos, silica, beryllium etc).
2. organic dusts
3. toxic gases
4. ionizing radiation
What is first affected in parenchymal restrictive disease?
first affects either the alveolar epithelial cells or the alveolar capillary endothelium
what is affected later?
What does interstitial damage lead to?
1. interstitial fibrosis/fluid leading to a stiffened lung and causing increased effort (dyspnea)
2. further damage to alveoli that leads to V/Q changes and thus hypoxia, leading to HTN and cor pulmonale
what is cor pulmonale?
RVH & RVF due to lung disease which causes pulmonary HTN
What happens in idiopathic pulmonary fibrosis:
-damage to type 1 alveolar cells
-fibroblasts are activated causing fibrosis of alveolar septa and arteriolar intima
What is the clinical course?
Fibrosis & pulmonary edema lead to decreased ventilation and hypoxemia. Decreased ventilation and pul. arteriolar fibrosis leads to pul. arteriolar vasoconstriction. Vasoconstriction leads to pulmonary HTN and cor pulmonale and death.
Who does hyaline membrane disease (aka infant respiratory distress syndrome)?
premature infants whose lungs have not matured to produce adequate surfactant
Whats the result of inadeqate surfactant?
high alveolar surface tension that leads to decreased lung compliance/dyspnea and atelectasis.
what are sn/sx?
decreased air movement heard on auscultation , tachypnea, cyanosis
What does CXR show?
bilateral atelectasis, hypoexpansion and domed diaphragms
On an amniocentesis, what are the indicators of a mature lung
-lecithin / sphingomyelin ratio > 2
-phosphatidyl glycerol is present
-antenatal corticosteroid administration to mother
-intratracheal exogenous surfactant to neonate: Exosurf Neonatal (colfosceril palmitate)
-combination of steroids to mother and surfactant to neonate has synergistic
Sn/Sx of ARDS?
-acute onset of respiratory distress
-decreased arterial pO2 and Hb O2-saturation
What does CXR show?
diffuse pulmonary infiltrates without evidence of left heart failure
Causes of ARDS?
1. sepsis/infection
2. Diffuse pulmonary infx
3. gastric aspiration
4. O2 toxicity
Which cells mediate injury to the alveolar capillary endothelium and the alveolar epithelium
neutrophils and macrophages
how is ARDS like hyaline membrane disease in infants?
development of hyaline membranes within the alveoli and alveolar ducts, decreased surfactant and resultant stiff lung and atelectasis
- dyspnea within 24 to 48 hours of injury or illness
-crackles, ronchii, weezing
-cyanosis which may not improve with O2 supplementation
How is diagnosis confirmed?
1. Labs: ABG shows acute respiratory alkalosis
2. CXR: shows diffuse bilat infiltrates (edema & atelectasis) similar to those of CHF, but heart is NL size
1. ABX if sepsis suspected
2. O2 supplementation
3. Persistent alkalosis should be reversed in order to enhance O2 offloading from Hb
What type of O2 supplementation works best?
-lung damage/hypoxemia is often refractory to O2 by face mask or nasal cannula
-intubate for O2 suppl. with PEEP (pos. end-expiratory pressure), or O2 via CPAP mask
what is mortality for ARDS?
currently about 50%, used to be 100%
What carries worst prognosis?
When can NL repiratory fx be expected if all goes well?
4-6 mos.
What is sarcoidosis?
a systemic disease characterized by non-caseating epithelioid granulomas in various organs. etiology unknown.
What are most common complaints of sarcoidosis?
-wt loss
What other systems are affected?
1. Skin-erythema nodosum and lupus pernio
2. Liver- granulomas present w/o clinical liver disease (i.e ALT/AST are NL)
3. Cardiac- dysrhythmias and/or CHF
4. Neurologic
5. Renal
How is renal system affected?
-renal failure
-hypercalcemia from either inc'd intestinal absorption of Vit D or inc'd conversion of Vit D to its active form within sarcoid granulomas
-renal calculi from hypercalcemia & hypercalcuria
How is it diagnosed?
1. hypergammaglobulinemia
2. PFTs show dec'd compliance, restrictive changes and dec'd DLCO
3. CXR shows bilateral hilar adenopathy and right paratracheal adenopathy = almost pathognomonic
4. Kveim test is positive
5. serum ACE levels significantly elevated
roids, but held off as long as possible b/c of adverse side effects
1. remit spontaneously
2. remain stable
3. progress
What is almost pathognomonic for sarcoidosis?
bilateral hilar adenopathy and right paratracheal adenopathy on CXR
What are the 3 main causes of pneumoconiosis?
asbestos, silicosis, and coal dust
What restrictive manifestations occur with asbestos?
ranges from pleural effusion to slowly progressing pulmonary fibrosis
Asbestos also inc's risk of what
Inc’d risk of lung CA and pleural mesothelioma ( benign or malignant)
what does lung histology show?
asbestos bodies, aka ferruginous bodies due to their gradual accumulation of protein and iron
what is mortality for ARDS?
currently about 50%, used to be 100%
What carries worst prognosis?
When can NL repiratory fx be expected if all goes well?
4-6 mos.
What is sarcoidosis?
a systemic disease characterized by non-caseating epithelioid granulomas in various organs. etiology unknown.
What are most common complaints of sarcoidosis?
-wt loss
What other systems are affected?
1. Skin-erythema nodosum and lupus pernio
2. Liver- granulomas present w/o clinical liver disease (i.e ALT/AST are NL)
3. Cardiac- dysrhythmias and/or CHF
4. Neurologic
5. Renal
How is renal system affected?
-renal failure
-hypercalcemia from either inc'd intestinal absorption of Vit D or inc'd conversion of Vit D to its active form within sarcoid granulomas
-renal calculi from hypercalcemia & hypercalcuria
How is it diagnosed?
1. hypergammaglobulinemia
2. PFTs show dec'd compliance, restrictive changes and dec'd DLCO
3. CXR shows bilateral hilar adenopathy and right paratracheal adenopathy = almost pathognomonic
4. Kveim test is positive
5. serum ACE levels significantly elevated
roids, but held off as long as possible b/c of adverse side effects
1. remit spontaneously
2. remain stable
3. progress
What is almost pathognomonic for sarcoidosis?
bilateral hilar adenopathy and right paratracheal adenopathy on CXR
What are the 3 main causes of pneumoconiosis?
asbestos, silicosis, and coal dust
What restrictive manifestations occur with asbestos?
ranges from pleural effusion to slowly progressing pulmonary fibrosis
Asbestos also inc's risk of what
Inc’d risk of lung CA and pleural mesothelioma ( benign or malignant)
what does lung histology show?
asbestos bodies, aka ferruginous bodies due to their gradual accumulation of protein and iron
What is silicosis?
intense lung inflammation and massive pulmonary fibrosis due to silica
what does CXR show?
eggshell calcification of hilar nodes
What causes pulmonary fibrosis in black lung?
coal dust itself causes no significant inflammation or physiologic dysfunction. Instead, it is the coal worker’s concurrent exposure to silica which causes the pulmonary fibrosis
Why is pulmonary BP low?
b/c pulmonary vascualar resistance is low
How can the pulmonary circuit accommodate large increases in cardiac output during exercise without a similar increase in its BP?
Because of its ability to recruit and dilate vessels
what is the pulmonary BP typically?
25/8 mmHg
Is pulmonary HTN easy to diagnose?
what are characteristics of primary (idiopathic) pulmonary HTN?
-progressive dyspnea
-rapid downhill course
-diffuse narrowing of pulmonary arterioles
Who does it mostly affect?
mostly young and middle-aged women
What causes 2ndary pulmonary HTN?
-Loss of pulmonary vessels
-Vascular obstruction
-Increased blood viscosity
What is the most important and potent stimulus for pulmonary vasoconstriction?
chronic hypoxia
What else causes vasoconstriction?
The cause of hypoxia is conditions that result in....
chronically poor ventilation
These conditions are:
-COPD i.e. emphysema, asthma, chronic bronchitis
-Obesity-Hypoventilation Syndrome
-Obstructive sleep apnea
-Neuromuscular disease
What happens as the resistance of the pulmonary circuit increases, due to vasoconstriction or one of the other causes?
the right ventricle
begins to strain, hypertrophy and eventually fail
What causes a loss of pulmonary vessels?
-pulmonary fibrosis
-autoimmune disease (rheumatoid, SLE)
What causes vascular obstruction?
-pulmonary embolism
-foreign bodies
-mitral stenosis
-constrictive pericarditis
what are sn/sx of pulmonary HTN?
Dyspnea, fatigue, chest pain or syncope on exertion, and narrow splitting of S2 with a loud P2
What is normal inspiratory splitting caused by?
increased negative intrathoracic pressure during inhalation that permits a momentary increase in venous return to the right heart, increased right ventricular filling, a slightly longer right ventricular systole and, therefore, slightly later closure of the pulmonic valve
What causes the narrow splitting of S2 in pulmonary HTN?
The right heart has chronic
difficulty ejecting its end-diastolic volume so closure of the pulmonic valve is delayed and slight (narrow) splitting may be heard
What causes a louder P2?
Since the pulmonary circuit is hypertensive, there is greater back pressure against the pulmonic valve, which slams it shut
more forcefully, causing a louder P2
What are the lab findings with pulmonary HTN?
What does ECG show?
-right atrial enlargement
-right ventricular strain
-right ventricular hypertrophy
What might V/Q scan show?
may show unmatched defects if pulmonary HTN due to recurrent pulmonary emboli
Are there any changes in PFTs?
no routine changes
-no effective Tx
-periodic phlebotomy if polycythemia and hematocrit > 60%
-prostacyclin (Epoprostenol) is a potent pulmonary vasodilator
What is bronchiectasis?
a pathologic expansion (ektasis ) of bronchi and/or bronchioles resulting from chronic necrotizing infections
Why is it considered a secondary disease?
b/c it's caused by infection caused by various conditions which destroy bronchial smooth muscle and elastic tissue
cough, expectoration of copious purulent, sometimes fetid sputum, and flecks of blood in sputum, if not frank hemptysis
-bronchial obstruction
-cystic fibrosis
What kinds of things cause obstruction?
-foreign body
-mucous impaction
This leads to what?
infx that causes bronchiectasis localized to obstructed segment only
What does bronchiectasis also complicate?
asthma and chronic bronchitis
What is cystic fibrosis?
an inherited autosomal recessive disorder of exocrine glands, primarily those of the respiratory and G.I. tracts
How does it lead to bronchiectasis?
causes production of very viscid mucus which causes recurrent infection leading to severe widespread bronchiectasis
CF causes a triad of:
-exocrine pancreatic insufficiency
-high sweat chloride content
How does HIV/immunodeficient states cause bronchiectasis?
they permit recurrent infections which leads to bronchiectasis
What are the 2 important factors that cause B?
obstruction and chronic or recurrent infx
which causes which?
both cause both:
-obstruction leads to dec'd NL clearance mechanisms leading to secondary infx
-infx can lead to obstructive secretions which can worsen infx and inflammation
Where does it usually affect?
lower lobes, esp. most vertical airways
What happens to the affected airways?
They dilate to 4x NL diameter; on gross dissection can trace severely dilated bronchioles almost all the way out to the pleura
T/F a single flora is usually cultured from bronchii?
F- mixed flora:
Staph, Strep, Pneumococci, H. flu, Pseudomonas
What often eventually happens?
lung abcesses
What does CT scan show?
dilated airways
What does CXR show?
inc’d bronchovascular markings
What causes these markings?
-peribronchial fibrosis
-intrabronchial secretions
CXR will show what part of lung to be affected?
apical or upper lobe
Sweat chloride test shows:
> 60 mEq/L chloride in kids
or >80 in adults
What do pt's often develop in the course of disease?
finger clubbing
clubbing is also seen with:
pts who smoke, have other lung diseases or lung CA, or have acute bacterial endocarditis.
What can result if B is severe and widespread?
obstructive ventilatory defects lead to hypercapnia / hypoxemia which causes pulmonary HTN, ultimately leading to cor pulmonale
abx to control infx, beta-2 agonists to maximize ventilation in non-bronchiectatic airways, respiratory therapy, and O2 therapy
What is atelectasis?
collapse of the alveoli in a lung segment; translates to "imperfect expansion"
Whats the diff between atelectasis and PTX?
Pneumothorax= collapse of alveoli is caused by separation of the visceral pleura from the parietal pleura
Atlectasis = other mechanisms cause the collapse
What are the 4 main mechanisms of collapse?
1 resorption
2 compression
3 contraction
4 diffuse microatelectasis
Obstruction in airway(s) prevents ventilation, so existing air in alveoli gets absorbed and they collapse
Where can it cause collapse?
one or more segments, a complete lobe, or an entire lung
What are typical obstructions?
-bronchus obstruction by mucus or mucopurulent plug (i.e. after surgery)
-foreign body (FB), esp. in kids
-tumor, esp. bronchogenic carcinoma
-enlarged lymph nodes, i.e. in TB
What is contraction atelectasis c/b?
caused by local or generalized fibrosis in lung or pleura
as cicatrization atelectasis
What causes compression atel.?
C/b something that nudges lung tissue out of the way or otherwise occupies space where lung normally resides
Examples that would do this?
1. pleural effusion
2. tumor
3. emphysematous bullae
4. cardiomegaly
5. elevated diaphram position (bedridden pt's or pt's with ascites)
What is diffuse microatelectasis?
generalized loss of lung expansion due to inadequate surfactant
-O2 toxicity = breathing high % O2 for TOO LONG
-neonatal or adult respiratory distress syndrome
-infection, which may cause adult resp. distress syn.
sn/sx of atelectasis?
-tracheal deviation
-uneven chest xpansion
-dec'd breath sounds
-dullness to percussion
after surgery encourage ventilation by:
-incentive spirometry
-early ambulation
What 2 conditions does COPD denote?
emphysema and chronic bronchitis
at least 80% of COPD is due to:
tobacco smoke, the irritant chemicals in which cause both excessive bronchial mucus secretions & chronic cough (chronic bronchitis) and destruction of acinar walls, with attending permanent enlargement of the acinar airspaces (emphysema)
What is emphysema?
permanent enlargement of airspaces distal to the terminal bronchioles, due to inflammation-induced destruction of the walls of the respiratory bronchioles,
alveolar ducts, and alveoli
What are the 3 histological types of emphysema?
-centriacinar (centrilobular)
-panacina (panlobular)
-distal acinar (paraseptal)
What part of lung is affected in centriacinar?
respiratory bronchioles are enlarged, common in lung apex; distal alveoli are spared
What part of lung is affected in panacina?
entire acinus is uniformly enlarged, usually at lung base
What is the acinus?
1 set of respiratory bronchioles, alveolar ducts, and alveoli
a genetic α1-antitypsinase deficiency
What part of lung is affected in distal acinar?
the far peripheral acini, close to the lung pleura, are enlarged
What can this type cause in young, tall, thin adults who've been smoking for awhile?
spontaneous pneumothorax
In the pathogenesis of emphysema, what causes acinar wall destruction
Excess lung protease and/or elastase activity, unopposed by anti-protease activity
What happens when acinar walls are destroyed?
-airspace enlargement
-loss of alveoli
-loss of alveolar capillaries
What results from airspace enlargement?
it means decreased total surface area for gas exchange
What else results from loss of structural integrity of acinar walls?
It leads to obstructive collapse on exhalation which causes air trapping & CO2 retention ultimately leading to hyperinflation of lungs
How does smoking cause alveolar inflammation?
by recruiting neutros and macros to alveoli
Sn/sx of emphysema?
-prolonged expiratory phase
-pursed lip breathing (“Pink Puffer” )
-pulmonary hyperinflation causes ∆ chest A/P ratio
-dec'd diaphragmatic excursion
- dec'd vesicular breath sounds
-distant heart sounds
-loss of alveolar capillaries
what does loss of alveolar caps lead to?
inc'd pulmonary vasc resistance and RH failure
Labs show:
-FEV1/FVC ratio < 75%
-dec'd FEF
-arterial pCO2 >40
Clinical course of emphysema?
-starts as DOE, then progresses to dyspnea upon resting
-weight loss (like CA pt)
What ultimately causes death in emphysema?
Chronic hypoxemia causes constriction of pulmonary arterioles leading to pulm HTN, and RV failure (cor pulmonale)
other complications?
repiratory acidosis and coma
-bronchodilators (anticholinergic inhaler or beta-2 agonist inhaler)
-inhaled roids
-O2 supplementation if severe
In O2 supplementation, what is the hypoxic drive and how do you maintain it?
- O2 supplementing can't exceed pO2 b/c central chemoreceptors (which drive resp rhythm generators by detecting inc'd pCO2) are desensitized leaving only peripheral receptors. Since the peripheral chemoreceptors are mainly responsive to decreased arterial Po2, excessive O2 supplementation ( arterial Po2 > 65 ) can decrease this hypoxic drive and put the COPDer at risk of a respiratory crisis.
- can't over oxygenate!
“Chronic bronchitis is defined by the presence of a:
- Mucus-producing cough, most days of the month
- 3 months of a year for two successive years without other underlying disease to explain the cough
What does inflammation lead to?
scarring of the lining of the bronchial tubes
What does prolonged scarring/irritation lead to?
excessive mucus production
which causes the lining of the bronchial tubes to become thickened and an irritating cough develops that can hamper air flow, possible scarring the lungs.
These conditions in the bronchial tubes are a precedent for what?
they become an ideal breeding place for infx
Besides smoking, what can chronic bronchitis and related emphysema also be caused by in the non-smoker?
by longterm exposure to air pollution in the form of dusts and chemicals.
Tx for chronic bronchitis?
stop smoking, avoid pollution, inhaled bronchodilator
COPD- over 40
asthma- younger, often in childhood
COPD-progressive dyspnea, cough, wheezing
asthma-variable dyspnea, cough and sputum
Allergic Etiology:
asthma-more than 50% have allergies, rhinitis, exzema, etc.
Response to Tx:
COPD-partial reversibility

COPD-poor response
asthma-good response
Which is characterized by cute (episodic) hyper-responsiveness of airways resulting in bronchoconstriction?
Can pt. engage in NL range of activities?
yes, except during episodes
How does pt. avoid asthma attack?
by identifying and avoiding allergic triggers
As a clinician, what would pt. say that will lead to rapid diagnosis?
having "bouts" of dyspnea (readily recalled)
How do sn/sx progress with COPD?
slowly, with little day to day variation--lifestyle modification over time
Are there "triggers" to what causes dyspnea?
Why can diagnosis of COPD be delayed?
b/c unlike asthma, pt. doesnt readily recall bouts of dyspnea
What is asthma?
an inflammatory lung disease characterized by
-airway inflammation without infection
-inc'd airway reactivity (bronchospasm & mucus ) to a variety of stimuli
-airway obstruction & acute dyspnea due to bronchospasm & mucus prod.
What happens during an asthma attack?
-bronchial edema
-inc'd bronchial mucus which causes airways to narrow causing dyspnea
What are the 2 major categories of asthma?
extrinsic and intrinsic
What is the trigger in extrinsic?
trigger for asthma attack is allergy / immune reaction
What are the 3 types of extrinsic?
Atopic (allergic), occupational, and Allergic Bronchopulmonary Aspergillosis
Which is most common?
atopic (allergic)
Which is c/b allergy to workplace dusts and pollutants?
How are sx alleviated in occupational?
leaving work
When is typical onset of atopic?
within first 2 decades
What is it also associated with?
other allergic (atopic) manifestations like rhinits, exzcema, urticaria (in both pt and relatives)
What do labs show in atopic?
inc'd serum IgE and inc'd blood eosinophil count
What happens in Allergic Bronchopulmonary Aspergillosis?
aspergillus fungus colonizes airways and there's an allergic response to it, causing inc'd serum IgE
Cryptogenic asthma is AKA:
what triggers intrinsic?
trigger is non-immune (non-allergic):
-cold exposure
-pulmonary infx
-inhaled irritants
Why is it often diff to distinguish btw extrinsic and intrinsic?
B/c patients with allergic asthma are often also susceptible to asthma attacks due to intrinsic triggers…exercise etc… due to their inherent tracheobronchial hyper-reactivity
What is the common denominator in all forms of asthma?
exaggerated bronchoconstrictor response--increased airway activity
How is inc'd airway activity determined?
by patient’s response to inhalation of histamine or methacholine
in allergic asthma, which cells in the bronchial tissue cause chronic inflammaion?
mast cells, eosinophils, lymphocytes
This is example of what?
type 1 hypersensitivity
What causes the release of primary and secondary chemical mediators of inflammation?
mast cell degranulation and activation
What are these mediators?
histamine, leucotrienes, prostaglandins, leucotriene B4, and eotaxin
What do prostas and leucos do?
inc'd vascular permeability, vasodilation, mucus secretion, and bronchoconstriciton
What does leucotriene B4 do?
recruits & activates eosinophils & neutrophils to secret more chem junk
What does Eotaxin from bronchial epithelial cells do?
-recruits & activates eosinophils
-Eosinophils produce more leukotriene C4
-leads to further mast cell activation
Is further exposure of allergen necessary for respnse to be sustained?
no, eosinophils that further activate mast cells sustains and amplifies the inflammatory response
In intrinsic, what causes bronchial inflammation and airway hyper-reactivity?
Viral URIs- a possible cause of the inflammation, also common air pollutants, such as ozone, SO2 and NO2
Sn/sx of asthma (both ex and in)
-Mild cough and wheezing
-nocturnal cough (in kids) is first sign
-then progresses to asthma "attacks"
What happens during an asthma attack?
-varying degrees of respiratory distress, with accessory muscle use
-audible wheezes on expiration, or during both expiration and inspiration
-coarse ronchii
-prolonged expiratory phase
-dry “tight” sounding cough during attack
What can happen as attack worsens?
-wheeze may disappear
-unable to speak more than a few words without stopping
-central cyanosis
-confusion / lethargy (suggestsrespiratory failure with CO2 narcosis)
What causes hyperventilation during an attack?
airway obstruction causes dec'd V/Q ratio, which causes hypoxemia, leading to hyperventilation
What happens to pCO2 early in attack (rarely measured)
What happens later in the attack as air is trapped?
-leads to inc'd residual volume leading to hyperinflation of lungs
-hypoxemia worsens (pO2 dec's)
-pCO2 inc's leading to respiratory acidosis
-FVC and FEV1 dec. progressively
What does CXR show during an asthma attack?
shows hyperinflation
This is also seen with...
The degree of what often correlates with the severity of asthma attack?
Eosinophilia can indicate one of 2 things:
-atopy (allergies) including allergic asthma
-parasite infx
inhaled steroids, Oral steroids, Leucotriene agonists, Mast cell stabilizers, and Bronchodilators
blocks inflammation during exacerbations:
oral steriods
blocks histamine component of inflammation:
mast cell stabilizers
usually for “rescue” from symptoms:
blocks leukotriene component of inflammation:
leucotriene agonists
blocks inflammation:
inhaled steriods
What are the 3 types of bronchodilators?
-Inhaled beta 2 (adrenergic)agonist
-Inhaled Anticholinergics
-Oral Xanthines
Which of these is used only for maintenance?
oral xanthines
What is normal extracellular Na+ concentration?
What is both intra- and extracellular H+ concentration?
Na+ concentration is how many times greater than H+ conc?
3.5 million times higher
For each 0.3 pH unit above 7.4, what happens to the [H+]?
it halves
For each 0.3 pH unit below 7.4, what happens to the [H+]?
it doubles
What is [H+] at pH 7.4?
40 nEq/L
Starting at base pH of 7.4 what happens when we both add and subtract .25 nEq/L H+?
add: pH becomes 7.19 and we live
subtract: pH becomes 7.82 and we die
So, what can we tolerate better, acidemia or alkalemia?
How can extreme acidemia lead to death?
Decreasing pH -->CNS depression --> coma -->death
How can extreme alkalemia lead to death?
Increasing pH -->Nervous system excitation
What does this do in the PNS?
paresthesias --> tetany --> respiratory paralysis --> death
What does this do in the CNS?
nervousness --> convulsions --> --> death
What is acidosis?
one or more physiologic aberrations that tend to produce too many H+ ions, or fail to remove enough of them, or cause loss of bicarb.
Does it always decrease pH?
not always- depends on what else is going on i.e. alkalosis
What is it called when acidosis causes pH to drop?
What is alkalosis?
one or more physiologic aberrations that cause accumulation of too much HCO3 and/or loss of too many H+ ions
Does it always inc pH?
no, depends on other conditions like acidosis
What is it called when alkalosis causes pH to rise?
What's the NL pH range of arterial blood?
7.4-7.44 (a 4 nanoMolar range)
What is acid-base status denoted by?
a set of numbers called the arterial blood gas, or ABG
pH is defined as:
the neg. log of the H+ concentration

pH = -log[H+]
How do you convert H+ ion concentration to pH?
Given: [H+] = 48nEq/L
1. type 0.000000048 and hit log
2. it shows -7.318
3. this means conc. = 10^-7.318 Eq/L
4. pH=7.318
How do you convert pH to [H+]?
Given: pH = 7.318
make it -7.318 and hit antilog
[H+] at pH 6=
[H+] at pH 7.1 =
[H+] at pH 7.4 =
[H+] at pH 7.7
what set of values comprises the ABG?
which of these are actual measurements made on the arterial blood
pH, pCO2, and pO2
how is HCO3 calculated?
by substituting the pH and pCO2 values into the henderson hasselbalch equation
What values are used to determine if a pt. has metab. acid., meta alk, resp acid., or resp. alk?
pH, pCO2, and HCO3
what is pO2 used for?
as an indicator of ventilatory status, but not for assessment of acid-base per se.
What else is measure along with ABGs typically?
routine serum electrolytes
what are they?
Na+, K+, Cl- and HCO3-
What is the hendersen-hasselbalch equation?
pH= 6.1 + log [(HCO3/(.03*pCO2)]
What are the NL values for HCO3 and pCO2?
HCO3= 24 mEq/L
pCO2= 40mmHg

(disregard units in calcualating)
When these values are put in the HH eq, what does pH come out to be (i.e. whats the NL ph)
How does HCO3 act as a buffer?
it's a chemical base that can accept an h+ ion to form H2CO3 which harmlessly dissociates removing the H+ ion and raising the pH. Intuitively, any increase in the qty. of base eliminates some acid and thereby raises or buffers pH against falling.
What happens when the numerator inc's (HCO3 inc's)?
the log of that fraction inc's beyond 1.3 and pH exceeds 7.4
How do kidneys regulate body pH?
1. inc/dec. reabsorption of HCO3 from tubular fluid
2. inc/dec. production of new HCO3
3. inc/dec. excretion of H+ into tubular fluid
How long does it take for kidneys to compensate when a pH disturbance occurs in healty kidneys?
few hours to begin adjustments, few days to reach max. effects
What can happen if kids are not healthy?
-kids may be the cause of pH disturbances
-diminished ability to compensate
what happens (in the HH eq) when pCO2 increases?
the log of the fraction dec's below 1.3 so pH falls below 7.4
how doe the lungs adjust pCO2
by blowing off CO2 in hyperventilation or by retaining CO2 in hypoventilation
what detects these pH disturbances?
peripheral and central chemoreceptors that then stimulate or inhibit the respiratory center in the medulla
What is the result of hypoventilation?
hypoventilation --> CO2 retention --> inc'd pCO2 --> dec'd pH
What does the excess CO2 create
volatile acid
What is the volatile acid in this case?
during hypoventilation, an inc in CO2 on the left drives the eq to the right producing:
H+ and HCO3-
Since both H+ and HCO3- are being produced why don't they balance out. i.e., why does pH still drop?
b/c chemoreceptors only respond to or "see" H+ ions and pH is defined as free [H+], not free HCO3
When does the body notice/benefit from the free HCO3?
only by its effect of the free [H+]:
-if there's enough HCO3 to combine with xs H+ to remove it and drive rxn back to the left
-if there's too much HCO3 (or too little CO2), rxn goes even more to the left and removes too much H+, inc'ing the pH
What happens when rxn goes back to the left?
H2O and CO2 are produced and CO2 can be exhaled, stabilizing or buffering the pH against xs acid
hyperventilation drives equation to the
what is the net effect of hyperventilation
removal of free H+ ions and their conversion to CO2, which is then exhaled
What causes hyperventilation?
1. extreme anxiety (involuntary)
2. pregnancy (causes rapid shallow breathing resulting in dec'd pCO2)
3. choose to (i.e. swimmers)
why do you feel dizzy when hyperventilating?
dec'd pCO2 causes cerebral arterioles to constrict which deprive head of O2
how do the kids compensate for hyperventilation?
dumping HCO3 in urine
In an acid base disturbance, whatever is compensating (lungs or kidneys), does the compensation ever return the pH to 7.4
what are 2 classic conditions that cause acid base disturbances?
1. severe diarrhea
What happens with severe diarrhea?
lg. qty of HCO3 is lost per rectum meaning there are more free H+ ions. plasma pH drops and lungs compensate by hyperventilating. kids compensate by making more HCO3-
What does COPD do?
causes hypoventilation and retention of CO2. plasma pH drops and kids compensate by conserving old HCO3- and by inc'ing excretion of H+ into urine
Respiratory acidosis:
primary change = inc pCO2
compensation = inc HCO3
Metabolic acidosis:
primary change = dec HCO3
compensation = dec pCO2
Respiratory alkalosis:
primary change = dec pCO2
compensation = dec HCO3
Metabolic alkalosis:
primary change = inc HCO3
compensation = inc pCO2
What causes respiratory acidosis?
Anything that induces hypoventilation resulting in CO2 retention and inc'd pCO2 (hypercapnea):
1. cardiac arrest
2. airway obstructions
3. thoracic pulmonary disorders
4. CNS related
5. neuromuscular
How does ca cause it?
b/c little/no blood is going to the lungs so theres no gas xchange
what causes airway obstructions?
foreign body, COPD
What are thoracic pulmonary disorders?
pulmonary edema, pneumonia, pneumothorax, pleural effusion
what are CNS related causes?
sleep apnea, CVA, drugs (morphine, heroin, sedatives, tranquilizers)
what are neuromuscular causes?
myasthenia gravis, muscular dystrophy, ALS, Guillan barre syndrome
What causes respiratory alkalosis?
Anything that induces hyperventilation and dec's pCO2:
1. anxiety (psychoneurosis)
2. pregnancy
3. asthma (early in attack)
4. high altitude
5. mechanical over-ventilation
6. encephalitis
what does high altitude do?
dec'd atmospheric pO2 causes "air hunger" and you hyperventilate to get more O2
what does encephalitis do?
overstimulates respiratory center in medulla
What causes metabolic acidosis?
inc'd acid production, acid ingestion, dec'd renal acid excretion and/or loss of HCO3-:
1. CArrest
2. severe diarrhea
3. ketoacidosis
4. renal failure
5. rhabdomyolysis
6. ingestions
what does card arrest do?
dec'd CO means dec'd O2 delivery to tissues resulting in lactic acid buildup
what causes ketoacidosis?
starvation or uncontrolled diabetes put fat catabolism into overdrive producing beta-hydroxybutyrate and acetoacetate. both dissociate to produce free H+ but acetoacetate also inhibits renal tubular reabsorption of HCO3
renal failure leads to
uremia and metabolic acidosis
rhabdomyolysis leads to
renal failure and metabolic acidosis
What things are ingested that cause metabolic acidosis?
ASA, ethanol, methanol, ethylene glycol
With the exception of diarrhea, all causes of meta acid. also do what?
cause in'd anion gap
What causes meta. alk?
Inc'd loss of acid:
vomiting, aldosteronism, diuretics
What does aldosteronism do?
adenoma of adrenal cortex causes inc'd aldosterone sec...this leads to ic'd renal Na reabsorption and in'd renal secretion of K+ and H+. in'd acid excretion means alkalosis
What do diuretics do?
like aldost.ism, they inc Na and H2O excretion causeing de'd circulatory fluid volume and BP which is detected by baroreceptors in kids....leading to renin-angio II-aldosterone pathway which in's H+ excretion
What is a simple acid-base disturbance?
-only one physiological abberation causing a pH change
-compensation is adequate
-i.e. compensatory change in HCO3 in response to primary change in pCO2 is always of a certain proportional magnitude and vice versa
What do the numbers look like in metabolic acidosis?
dec'd pH, dec'd pCO2, and dec'd HCO3
What do the numbers look like in respiratory acidosis?
dec'd pH, inc'd pCO2 and inc'd HCO3
What do the numbers look like in metabolic alkalosis?
inc'd pH, inc'd pCO2, dec'd HCO3
What do the numbers look like in respiratory alkalosis?
inc'd pH, dec'd pCO2, dec'd HCO3
How do you determine if it's a simple acid base disturbance based on the numbers?
by comparing the expected compensatory change to the observed (if it's within 2-3 units, then ok)
How do you determine if it's a mixed acid-base disturbance?
if at any time the observed compensatory level is more or less than the calculated expected level, there's a secondary disturbance
Compensation in metabolic acidosis:
dec in pCO2
Compensation in metabolic alkalosis:
inc in pCO2
Compensation in respiratory acidosis:
inc in HCO3
Compensation in respiratory alkalosis:
dec in HCO3
in mixed disturbances, what causes inadequate compensation?
lung or kidney problems
what are 2 distinct types of mixed disturbances?
1. two opposing aberrations that leave pH at 7.4
2. two aberrations in the same direction and no compensation
respiratory acidosis and metabolic alkalosis
What combo of conditions/problems would cause resp acid and meta alka?
has COPD (high pCO2) and is on diuretic (high HCO3)
pCO2= 54
respiratory acidosis and metabolic acidosis
uninterpretable due to technical or human error
Severe alkalemia in 1st trimester of pregnancy due to hyperventilation and vomiting (HCl):
Metabolic alkalosis and respiratory alkalosis
COPD plus diuretic therapy for systemic HTN:
Metabolic acidosis and resp acid
Dangerously low pH due to cardiopulmonary arrest:
Metabolic Acidosis & Respiratory Acidosis
Critically ill patient hyperventilating, who also has alcoholic ketoacidosis, or sepsis and --> massive vasodilation -->↓ systemic pressure & flow --> lactic acidosis:
Metabolic Acidosis & Respiratory Alkalosis
Severe Gastroenteritis:
-vomiting HCL --> alkalosis
-diarrhea --> acidosis
Type I Diabetes: nausea and vomiting preceding ketoacidosis
-vomiting --> alkalosis
-ketoacid accumulation --> acidosis
Metabolic Acidosis & Metabolic Alkalosis
critical pH values:
< 7.25
> 7.55
critical pCO2 values:
< 20
> 60
critical HCO3 values
< 15
> 40
critical Arterial pO2:
< 40
critical O2 Sat. :
< 75%
What two things does the anion gap facilitate?
1. Identification of metabolic acidosis even without benefit of a pH value
2. Suspicion that an identified metabolic acidosis is due to accumulation of acid...
methanol, aspirin, propylene glycol, lactic acid etc…rather than G.I. loss of HCO3
What is the anion gap calculated from?
the “routinely measured plasma ions” Na+, K+, HCO3- and Cl-.
What is the charge in the plasma in which these 4 ions float?
it's electrically neutral, no net charge b/c the electrical sum of all anions and cations is zero
Na+ and K+ account for how much of all the positive charges in the plasma?
Do the HCO3- and Cl- ions constitute all the negative charges in the plasma?
What else makes up plasma's neg charge?
albumin, HSO4- etc.
What happens if we subtract the sum of the milliequivalent concentrations of the HCO3- & Cl- ions from the sum of the Na+ & K+ ions?
we normally get a positive number, rather than zero
What are the classic normal mEq/L concentrations of the four ions?
Na+ = 140
K+ = 4
HCO3- = 24
Cl- = 104
What is the NL anion gap?
(140 + 4) - (24 + 104) = 16 (plus or minus three.
What is the NL anion gap using the potassium-less formula?
12 (plus or minus 3)
What is the only acid-base disturbance in which change in the anion gap is of clinical importance?
metabolic acidosis
What happens to the anion gap in metabolic acidosis?
it inc's
b/c excess acid in person's body (i.e. lactic acid) combines with HCO3- so there's less HCO3- in the plasma.
What else is this called?
increased anion gap metabolic acidosis or anion gap acidosis
Why is it of clinical importance in metabolic acidosis?
When metabolic acidosis exists, detection of a normal anion gap, or an increased anion gap, helps narrow the possible causes of the acidosis
If the gap is NL, what could be the possible causes of meta acid?
diarrhea, renal tubular acidosis, fistulae, carbonic anhydrase inhibitor
What are the two types of causes of anion gap meta acid?
exogenous and endogenous
what are the exogenous causes?
aspirin, ethanol, methanol, and ethylene glycol
what are endogenous causes?
lactic acidosis or ketoacidosis (diabetes/starvation)