Pulmonary vascular disorders Flashcards
what is pulm edema
fluid accum in alveoli (theres always a small amount of fluid there)
et of pulm edema
usually left sided heart failure
- non cardiogenic
- IV fluid overload
- smoke inhalation
- aspiration
- IV drug abuse (recreational)
how does smoke inhalation affect pulm edema
toxic fumes such a from fire bring inflm which changes permb and leads to fluid int he alveoli
how does IV drug abuse contribute to pulm edema
there is inc permb and CNS depression of resp and circ fx
patho of pulm edema
Fluid from blood to IS to alveoli leads todec resp function
(In order to move across for gas exchange, O2 and CO2 need to be able to dissolve into the fluid between the capillary and the alveoli…with PE, fluid is added into this space expanded diffusion distance + also taking up space that air would otherwise occupy in alveoli)
mnfts of pulm edema
- cough
- productive (frothy, blood tinged)
- dyspnea
- dec lung compliance (like inflating balloon in it)
- crackles
tx of pulm edema
- resp support
- cause eg inc heart fx
pulmonary embolism occurs where? what is it?
- Thrombus in the pulmonary vessel (will be an ARTERY)
- Potentially lethal – (if is one of larger arteries, will be about ~1/3 death rate. MI is same thing in pulmonary circuit)
- 10% recurrence rate (problem returns at later date)
which side of the pul circuit will the emboli come from
R side (from heart)
et of pulm embolus
•Usually from DVT (in veins
-Iliac, popliteal, or femoral V
•Other emboli:
o Fat – could come from bone marrow if you have fracture (sever blood vessels which have marrow adjoining, fat enters circulation here)
o Air (through IV, injection)
o Amniotic fluid:( during birthing process, these membranes rupture and release amniotic fluid….also during labour and birth, vessels are severed and burst…
Here talking about the particulate matter in the fluid, not the fluid itself)
• Saddle embolus = embolus settles in “saddle” formed by bifurcation of the pulmonary artery
patho of pulm embolus
- DVT –> embolus –> thrombus in arterial bed –> impaired perfusion
- Ventilation : perfusion imbalance –> hypoxemia
- Platelets degranulate(mediators released) –> bronchial and pulmonary artery constriction –>hemodynamic instability (= blood volume, pressure, and flow)
- Reflexive bronchoconstriction (SNS response)
- Dec in cardiac output (d/t thrombus occluding pulmonary artery so little blood returning to the left side of the heart)
- L/o surfactant–>atelectasis
- Right-sided heart failure possibly results
what is worse hypoxemia from pulm embolus of embolus itself
embolus
why does a loss of surfactant and atelectasis result from pulm embolus
1) Any secretion from a gland requires adequate perfusion;
2) Even if perfusion is partial or relatively adequate, whenever there is some impact in perfusion, you have ischemic damage to these cells
why can R side of heart fail with PE
what could result from this
heart is pumping against inc resistance which will cause hypertrophy and failure
LSHF could result but generaly there will be intervention before this stage
mnfts of PE
• Based on size and site
• Usually: chest pain, tachypnea, dyspnea(Ahmed says we will NOT be able to explain these!)
o Chest pain d/t Ischemia
o Tachypnea d/t resp system working in concert with cardio system…one is failing, the other is attempting to compensate. Also may have bronchoconstriction
• Tachycardia - compensatory response for dec’d CO
dx of pulmonary embolus
- Hx and px– could be MI for all we know.
- ABG
- LDH3
- Lung scan (131 I-HSA, IV)
- CT, Chest xray
- Pulmonary angiogram
what is LDH3
(Lactate Dehydrogenase, enzyme released when there is damage to the lung tissue (d/t infarction from ischemia) )
o #3 says is subset of other LDH…like subclasses of CKMB, BB, etc.
what is the lung scan and how does it relate to pulm embolus
what can it tell us
lung scan (131 I-HSA, IV) –( HAS is marked albumin (??Double check this???), protein is labeled with Iodine 131; a radio isotope used to tag compounds;
o Will show you if you have a larger obstruction
o Albumin marked with isotope injected
o This is non invasive procedure )
what is more definitive lung scan or pulmonary angiogram
pulm angiogram (camera on catheter threaded into pulmonary circuit; this is more definitive than HAS, but is invasive)
tx of pulm embolus
• STAT treatment improves prognosis
- Anticoagulants and thrombolytics
- Maintain cardio-pulmonary function (avoids shock)
• Treat DVT
what is pulm HTN
what is it similar to
- Sustained pressure inc in pulm circuit (>25 mmHg; normal ~15)
- Is like portal hypertension in that is confined to the pulmonary system
what is the pulm circuits P like
• Pulmonary circuit
o Is low pressure, low resistance circuit. ( has many paths as vessels disseminate, so as progress into capillary beds, pressure drops)
Analogy of cars leaving highway…if more streets to follow,
If cardiac output increases, will be slight increase in pressure of the circuit, but should not cause any significant inc in pressure (vessels should be able to handle that inc)
If traffic increases, and then you also have a bunch on construction, then going to be lots of backup of traffic
how does an inc in CO affect the pulm circuit
what affects the P in this circuit
o If CO inc -> minimal inc in pulmonary pressure
pulmonary vasoconstriction->inc P
et of pulm HTN
-occur secondary to crdiac and pulm problems
3 kinds
1) inc in pulm volume eg cardiac septal defects
2) hypoxemia
3) inc pulm venous P (eg left ventricular dysfx)
how is inc pulm volume (eg cardiac septal defects et factor for pulm HTN)
septal defects the fetal blood doesnt cycle through the lungs which is partially achieved by having opening of septum between RA and LA so blood is channeled through this and out through aorta
with a septal defect incomplete closure means more blood is being sent through the lungs
how is hypoxemia an et factor for pulm HTN
if tissues are deprived of O2 the vessels respond by dilating. In other tissues the oxygen comes from the lungs but with this hypoxemia in the lung tissue itself the lung vessels actually vasocontrict in an effort to localize the accum of CO2 instead of causing widespread hypoxemia
how is inc pulm venous P (L ventricular dysfx) an et factor in pulm HTN
with L sided heart failure there is pooling of blood in the LV then LA then pulm circuit. The volume inc brings an inc in P
reveiw fetal circ
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fetal circ
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fetal fir
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mnfts of pulm HTN
- dyspnea, syncope and chest pain on exertion
- mnfts of right sided heart fail
- on CXR we’d see 2 things if severe
1) Rventricular hypertrophy
2) distended pulm arteries - fatigue
why do chest pain and syncope occur w pulm HTN
nt really explainable
theres no ischemia for chest pain and the syncope gen occurs when theres a loss of blood flow, glucose, O2 to brain
tx of pulm HTN
- Is very difficult!
- Cause
- Vasodilators ( caution, will cause systemic vasodilation)
- Dec prognosis if severe
what does ARDS stand for and what else is it acceptable to be called
acute resp distress syndrome
or ca be called post traumatic lung
what is acute resp distress syndrome
whats the mortality rate
• Severe damage to alveolar & cap walls
o Acute onset, rapidly progresses (d/t fire, drowning, etc)
• 40-60% mortality
et of ARDS
• Aspiration (anything other than air into lungs) • Excessive smoke inhalation (from fire) • Fat embolus • Septicemia (bacteria enter and survive in the circulation, causing serious problems throughout the body) • Drugs: cocaine, heroin • Severe burns • Near drowning -disseminated intravascular coagulation -breathing high conc of O2
-
mechanisms of lung changes in ARDS pg 703
o Damage to resp system Vasodilation + inc cap perm mediators released exudate formation
o Non-defensed cells + proteins and cells move in en masse as damage to the alveoli allows entry (this is an increase of permability in a pathological sense)
o Leukotrienes release Platelet Aggregating Factor (cause platelets to party in the alveoli), Proteases
o Exudate begins to form wall along the lining of the alveolus…this is hyaline??
patho of ARDS how does impaired as exchange occur
- lung trauma–>neutrophil influx–>free radicals, phospholipids and proteases–>endothelial and alveolar damage–>inc permb–>efflux of proteins, cells, and fluid into IS and alveoli–>edema–>dec lung compliance and impaired gas exchange
- surfactant deficiency and inactivation–>atelectasis
- thick protein and cell rih exudate lines alveoli–>no gas exchange
- impervious hyaline membrane lines alveoli
- profound hypoxemia
how is ARDS similar and different than pulm edema
there is a lg vol of fluid in ARDS and you cant reverse the issue
why use hyaline to describe the impervious hyaline membrane that lines alveoli
because it is hard and impermeable
mnfts of ARDS early stages
- acute onset resp distress
- dyspnea
- tachypnea
- inc hypoxemia
- resp alkalosis
late stages of ARDS mnfts
late metb acidosis
-diffuse consolidation
how is metb acidosis a late stage of mnfts of ARDS
its r/t the hypoxemia–>anaerobic metb and a buildup of lactic acid
what is lung consoidation in ARDS
exudate and fluid, debris, and cells solidifiy and this is consolidation
tx of ARDS
early intervention
- reverse cause
- resp support
- complications
lung cancer is it primary or secondary
can be both
is a preferred secondary site because it is large and richly perfused
mortality and lung CA
major cause of death
moratily rate is 30-35%
char of lung CA in terms of course
aggressive invasive and metastatic
where does lung CA spread
bones
liver
brain
how is lung Ca divided into types
-adenocarcinoma 30%
-squamous cell carcinoma 30%
-large cell carcinoma 12%
all the above 3 are non small lung CA- NSLC
small cell carinoma 22% SCLC
et of lung CA
-smoking >80%
toxins eg asbestos
-genetic predisposition
patho of squamous cell carcinoma
arises in central bronchi (hilum)
- spreads to hilar nodes
- more common in men
95% of lung CA originates from
it is bronchogenic
what could squamous cellc carcinoma affect
the heart d/t external P
who are squam cell carcinomas more common in
men
adenocarcinoma originate where
common in?
peripheral origin
alveoli or bronchioles
commmon in women and nonsmokers
lg cell carcinomas origin?
what else is unique
peripheral origin
- lg undifferentiated cells
- early metastasis
- poor prognosis (relative to other NSLC)
small cell carcinooma
most common in
origin
99% in smokers
aggressive, invasive, early mets (esp to brain) (also locally invasive
-small oval cells
-mets at dx
-non resectable
-radiosensitive
paraneoplastic syndromes eg SIADH and cushing’s (cortisol and ACTH)
which type of lung Ca would be hardest to excise
small cell carcinoma
which type of lung CA is more common in nonsmokers
adenocarcinoma (also comon in women
which lung CA arises in central bronchi
squam cll carcinoma
wich type of lung CA are likley to have metastasized
large cell carcinoma has early metastasis
small cell carcinoma has metastasized at dx
what are paraneoplastic syndromes
instead of ectopic tumours we have these syndromes eg SIADH and CUshings
mnfts of lung CA are based on
type site extent metastasis paraneoplastic syndromes
mnfts of lung CA
if central->impairs ventilation->coughing (unexplained), wheezing, dyspnea
- hemoptysis (d/t damaged blood vessels
- pain
- cardiac mnfts
