Pulmonary Restrictive Flashcards
1
Q
What is restrictive lung disease?
A
- Inspiration is limited → reduced compliance of the lung or chest wall = “stiff lungs”
- Ex: Can be anatomical chest wall probs or compliance of lung tissue themselves
- Reduction in lung compliance = increased work of breathing and dyspnea
- Rapid, shallow breathing pattern is observed = increased dead space ventilation
- Inc WOB nec to expand poorly compliant lungs. Hypercarbia = often worse during sleep bc pt loses the conscious awareness of a need to compensate w/ inc RR
- Normal gas exchange .. .. (not nec something wrong w/ alv)
- … Until advanced disease → increased PaCO2, decreased PaO2 → with pulmonary HTN, and cor pulmonale
- Increased work of breathing is necessary to expand poorly compliant lungs. Hypercarbia is often worse during sleep because the patient loses the conscious awareness of a need to compensate with increased RR
2
Q
What are lung volumes like in restrictive lung disease?
A
-
Reduction in:
- Total lung capacity
- Functional Residual Capacity
- Reserve Volume
- Vital capacity (nml >70mL/kg)
- FEV1 (forced expiratory volume 1 second)
- FVC (forced vital capacity)
- Total volume exhaled
- In pic- the lung vols are dec, see dec VT, VC, ERV, FRC, & TLC
-
No change in:
- Expiratory Flow Rates – no impedance to expiratory phase of flow volume loops → no change in exp flow rates
-
FEV1/FVC ratio normal
- Both volumes smaller → ratio remains normal
- Everything decreased
3
Q
Classsification of restrictive lung disease?
A
- Acute Intrinsic (ex: pulmonary edema)
- Chronic Intrinsic (ex: diseased lung parenchyma - fibrosis)
- Chronic Extrinsic (ex: chest wall, intra-abdominal & neuromuscular diseases)→ outside of the lung tissue itself
- Disorders of the Pleura and Mediastinum – tend to be more anatomical
4
Q
What is pulmonary edema?
A
Acute intrinsic restrictive disease
- Fluid leakage from the intravascular space into the lung interstitium and alveoli
Caused by:
- Increased capillary/hydrostatic pressure (example: cardiogenic)
- Inc in vascular pressures that causes fluid to leave caps & enter lung tissue
- Increased capillary permeability (d/t underlying inflammatory process)
- Allows fluid to be released from caps into lung tissue
- Pulm edema caused by inc cap perm is characterized by high conc of protein in the edema fluid and evidence of secretory products d/t an underlying inflammatory process.
- Allows fluid to be released from caps into lung tissue
CXR will show bilateral symmetrical opacities
- lungs filled w/ fluid
- Diffuse alveolar damage is descriptive of inc perm pulm edema typically associated with ARDS.
- CXR characteristic of cardiogenic edema is the “butterfly” pattern or a perihilar distribution of opacity
Causes of pulmonary edema: ARDS, Aspiration Pneumonitis
5
Q
What is ARDS?
A
Acute respiratory distress syndrome- acute intrinsic restrictive disease assoc w/ pulmonary edema
- Diffuse pulmonary endothelial injury
- H2O, solutes, and macromolecules → diffuse from intravascular space/capillaries into lung parenchyma and alveoli
- Often underlying inflammatory process: →
- Sepsis (bacterial or viral) often co-exists → producing further lung injury via inflammatory mediators
- Often ARDS signals the beginning of multiple organ system failure (MODs)
- MODS = hyper-dynamic, hyper-metabolic state similar to sepsis
- lungs are usually 1st organs to fail followed by liver, kidneys, GI tract (no longer acts as a barrier to bacteria for systemic circulation), and heart (ventricular wall motion abnormalities).
- With 3 organs involved→ mortality often 100%.
- lungs are usually 1st organs to fail followed by liver, kidneys, GI tract (no longer acts as a barrier to bacteria for systemic circulation), and heart (ventricular wall motion abnormalities).
- Ex rn = COVID pts getting ARDS → lungs first under stress → then progress to MODS quickly
- MODS = hyper-dynamic, hyper-metabolic state similar to sepsis
6
Q
What is aspiration pneumonitis?
A
Acidic gastric secretions destroy surfactant-producing cells & damage the pulmonary capillary endothelium
- Similar to ARDS – increased permeability pulmonary edema with atelectasis
- w/ anesth, lose reflexive mechs and can aspirate gastric contents into lungs
Clinically, the patient will demonstrate:
- Hypoxia: SpO2 < 92%
- Tachypnea
- Bronchospasm → wheezing
- Pulmonary vascular constriction → develop into pulmonary HTN
- (shunt blood from areas not ventilated to areas they are)
- Usually a good thing unless have this occur in a large part of lung – the constriction then leads to PHTN & can lead to further hydrostatic extravasation of fluid into lung tissue too
-
**CXR changes 6-12 hrs later – usually right lower lobe (LLL lower and will most likely go to R side)
- All you can do at the time is provide support- O2, may need to reintubate & ventilate until it resolves.
7
Q
What is the treatment for aspiration pneumonitis?
A
- #1 treatment is delivery of increased FiO2
- PEEP- keep lung tissues open
- b-2 agonists for bronchospasm
- +/- lavage of 5ml NS controversial
- may dilute the gastric contents→ w/ low pH and allow for easier suctioning – on the down side lrg vols of fluid may exac the spread of gastric fluid & rapidly distribute to peripheral lung areas
- Fiberoptic bronchoscopy
- if suspected solid material aspirated, usually d/t gastric contents tho
- Antibiotics, steroids? → controversial
- Corticosteroids and preventative abx are controversial and have not shown to really benefit patients but are often given anyways
- Albumin
- also controversial. Pts often have low albumin bc of leakage of plasma prot into lungs, but some suggest that giving albumin just makes this process worse & hypoalbuminemia should just be tolerated.
8
Q
What is cardiogenic pulmonary edema?
A
- Left ventricular failure with increased pulmonary vascular hydrostatic pressures
- L side of heart fails & activates SNS & RAAS → leading to massive vasoconstriction & fluid vol shifts
- Causing cap perm ability to be inc (not bc of underlying inflamm but bc of true hydrostatic pressure changes).
- L side of heart fails & activates SNS & RAAS → leading to massive vasoconstriction & fluid vol shifts
-
Signs of SNS activation usually more dramatic than with increased capillary permeability edema
- Extreme dyspnea
- Tachypnea
- Hypertension
- Tachycardia
- Diaphoresis
9
Q
What is neurogenic pulmonary edema? Treatment?
A
- Occurs minutes to hours following an acute brain injury (medulla, especially)
-
Secondary to massive SNS discharge in response to CNS insult
- Generalized vasoconstriction w/ shift large blood vol into pulmonary vessels = vessel injury & transudation of fluid into lung parenchyma/alveoli
- Similar to cardiogenic form
- Doesn’t occur in every pt w/ an acute brain injury – only a sm #.
- You should always have the possibility in the back of your mind however as the symptoms will often show up in the peri-operative period.
-
Treatment is supportive for both cardiogenic & neurogenic.
-
*Control ICP elevations, increased FiO2, PPV, PEEP, etc.
- Diuretics not indicated
- Resolution of edema occurs within a few days as brain inj settles down
-
*Control ICP elevations, increased FiO2, PPV, PEEP, etc.
10
Q
What is drug induced pulmonary edema?
A
Heroin – high permeability type
- smoking heroin causes damage to caps & lung tissues
- Fluid leaves capillaries and into lung tissue
Cocaine – pulmonary vasoconstriction and/or MI can result in pulmonary edema
- coke = sympathomimetic → so get inc in hydrostatic pressure (SNS activity) → pulm edema
- Treatment is again:
- supportive – vent, PEEP, Inc FiO2, etc
- Treatment is again:
11
Q
What is high altitude pulmonary edema?
A
- Mechanism believed to be intense hypoxic pulmonary vasoconstriction after 48-96 hours at 2500-5000m altitude
- (rapid ascent)
- Decrease O2 high altitudes→ hypoxic pulmonary vasoconstriction → bc its all over the lung →
- Increased pulmonary vascular pressures result in high permeability pulmonary edema
- Fluids go out into tissue
- Treatment:
- O2, prompt descent from altitude, and inhaled nitric oxide (bronchovascular dilator)
- NO: bronchodilates & vasodilates the constricted vessels so fluid can go back into the vasculature & out of the lungs
- O2, prompt descent from altitude, and inhaled nitric oxide (bronchovascular dilator)
12
Q
What is re-expansion pulmonary edema?
A
- Enhanced capillary membrane permeability – when previously collapsed lung re-expands
- Occasionally follows evacuation of pneumothorax or pleural effusion
- Lung expands back really quickly → permeability changes as a result
- More common if >1L fluid/air in pleural space, >24 hour duration of collapse, and if re-expansion occurs rapidly
- Supportive treatment, no diuretics
- Resolves within a few days (no diuretics)
- Vent, PEEP, increase FiO2
13
Q
What is negative-pressure pulmonary edema? Cuases?
A
- Occurs minutes to 2-3 hours after acute upper airway obstruction in a spontaneously breathing patient
- Causes:
-
Post-extubation laryngospasm
- They try to br against closed glottis, can gen enough neg pulm prs that causes hydrostatic extravasation of fluid from caps into alv
- Obstructive sleep apnea – if severe enough
- Epiglottitis
- Tumors
- Obesity
- Hiccups
-
Post-extubation laryngospasm
14
Q
Pathophys behind negative-pressure pulmonary edema
A
Development related to generation of highly negative intrapleural pressures against a closed glottis/upper airway
- Decreased interstitial hydrostatic pressure
- Increased venous return
- Increased afterload on left ventricle
- Increased SNS outflow – HTN, central pooling
- Hypoxemia with further SNS activation
- all of these factors together are thought to inc transcapillary prs gradients along w/ arterial hypoxemia and the assoc SNS stim
- Ex: Extubate pt or epiglottitis, glottis narrows or closes & pt tries to generate a breathe, causing extravasation of fluid from caps into lungs, lungs start to get filled w/ fluid that then causes shift in fluid status, coming to venous return of heart, with inc SNS, causing further vasoconstriction & worsening of both Preload & Afterload to heart.
- Prob will have to reintubate pt & allow situation to resolve which it will within 24-48 hrs & provide supportive care
- Easy to confuse symptoms w/ PE or aspiration. Subtle neg prs pulm edema may be to blame for many desaturations in immed post-op per
15
Q
s/s and treatment negative pressure pulmonary edema
A
- Tachypnea, cough, failure to maintain SaO2 >95%
- Usually self-limited – 12-24 hour duration
- Treat with supplemental O2, maintenance of airway, and if necessary mechanical ventilation
16
Q
Overview chronic restrictive lung disease?
A
- Pulmonary HTN and cor pulmonale are likely as progressive fibrosis = loss of pulmonary vasculature
- Pneumothoracies → common with advanced disease
- Why need resections and transplants
- Pneumothoracies → common with advanced disease
- Dyspnea prominent – rapid and shallow breathing leading to further probs (atelectasis) Viscous cycle.
17
Q
Pathogenesis of chronic restrictive lung dx?
A
* Lung injury from antigen/exposure = activates macrophages → fibrogenic and chemotactic cytokines released and recruitment of neutrophils → leads to oxidants/proteases that destroy type 1 pneumocytes (hypertrophy) → eventually hypertrophy and hyperplasia of type 2 pneumocytes
can be lung inj from someone w/ LT asthma, eventually gets lung inj or ie recovering from covid 19 but have lung inj, or LT smoker.
18
Q
What is relationship b/w pulm HTN and cor pulmonale?
A
- if you can do effective treatment @ increased PA pressures, can prevent the progression further. But if that doesn’t happen, it continues
- * Pathogenesis of pulmonary HTN and cor pulmonale caused by disease of the respiratory system or hypoxia
19
Q
What is sarcoidosis?
A
- Systematic granulomatous disorder; often found in thoracic lymph nodes and lungs
- Ex: Liver, spleen, optic, and facial nerve often involved
- Develop Cor pulmonale and pulmonary HTN likely
- Decreased alveolar diffusion capacity
- Granulomas settle in/found in alveoli and lung tissue
-
Laryngeal sarcoid 1-5% of patients
- can interfere with passage of ETT
-
Myocardial sarcoid (rare)
- Causes heart block, dysrhythmias, restrictive cardiomyopathy
- see these effects if on R side of heart, esp near RA
- Causes heart block, dysrhythmias, restrictive cardiomyopathy
20
Q
What to watch for with pt with sarcoidsois? DX? What might you need to give them perioperatively?
A
-
Patients often present for mediastinoscopy for diagnosis
- take a sample of thoracic lymph node for biopsy and diagnosis of sarcoid
- Watch for hypocalcemia
-
Patient may need a stress dose of steroids peri-operatively – often on chronic corticosteroids for treatment FYI
- Minor surgery – 2x normal dose steroid
- Moderate surgery – 25mg hydrocortisone pre-op, 75mg IV hydrocortisone intra-op, 50mg IV hydrocortisone post-op – taper to normal dose
- Major surgery – 50mg IV hydrocortisone pre-op, 100mg IV hydrocortisone intra-op, 100mg IV hydrocortisone post- op Q8 hours x24 – taper to normal dose
21
Q
Overview of chronic extinsic restrictive lung disease?
A
2 types:
-
Compressed lungs
* result in increased WOB
* Decreased lung volumes with corresponding increase in airway resistance
-
Compressed lungs
-
Abnormal chest wall mechanics
* With thoracic deformity→ Right ventricular dysfunction common with chronic compression of pulmonary vasculature
* Impaired cough = chronic infection, development of obstructive component
-
Abnormal chest wall mechanics
- → Cant exchange air bc of restriction on lungs
- cant cough, cant take deep breaths appropriately, & can lead to mucous settling in the lungs & cause chronic infections (start to like COPD pts and get obstructive lesions)
22
Q
Obesity and restritive lung disease?
A
- Diaphragm and chest wall movement restricted by excessive weight/ abdominal panniculus
- Dyspnea especially w/ exercise - increased resistance to breathing and increased work to move excess weight off their chest & abd area w/ mvmt of diaphragm
-
FRC decreased with V/Q mismatch
- can be severe in very obese & lead to hypoxia, hypercarbia, acidosis, etc
- Supine position exacerbates
- tend to use multiple pillows to sleep at night to help diaphragm expand
25
Q
What is flail chest?
A
- Secondary to rib fractures/sternotomy dehiscence (cardiac surgery)
- Paradoxical inward movement of the unstable portion of the thoracic cage during inspiration
- Ex: when inhale (instead of lung expanding in areas affected)→ lung will collapse
- When exhaling (area affected) → will increase in size
- Lung increases volume during exhalation and decreases volume during inhalation
- → Decreased PaO2 & increased PaCO2 secondary to alveolar hypoventilation
- Paradoxical inward movement of the unstable portion of the thoracic cage during inspiration
- Tx: Positive pressure ventilation required until thoracic cage stabilization occurs
- usually surgical intervention to fix cause
- Normal respiration: A, inspiration; B, expiration.
- Paradoxic motion: C, inspiration, area of lung underlying unstable chest wall sucks in on inspiration, Note movement of mediastinum toward opposite lung during inspiration
-
D, expiration, unstable area balloons out → air gets into area that’s impacted & sits there, so theres co2 there & doesn’t take good part in exchange
- see in trauma to chest, need intubation, vent, & surgical correction
40
Q
What are flow volume loops like in asthma? ephysema?
A
- Asthma - lung vol in pretreatment – top portion exp and bottom insp.
- Expiratory flow very diminished.
- If give them an inhaler or beta agonist → can increase their normal exp flow & insp flow
- “reactive” COPD- reversal of reactivity
- Expiratory flow very diminished.
- Emphysema
- Fixed COPD (emphysema) – even post treatment w/ inhaler won’t help
- exp flow still diminished
42
Q
Pathogenesis of pulmonary embolism?
A
* Pathogenesis of massive pulmonary embolism caused by a thrombus (pulmonary thromboembolism)
- Hypercoag →
- can be genetic, smokers, birth control pills w/ higher doses of estrogen.
- Typically genetics do play a role
- can be genetic, smokers, birth control pills w/ higher doses of estrogen.
- Thrombus formation → Dislodgement of portion of thrombus (from pt moving, inc in BP or inc in flow thru that vessel)
- Thrombus occludes portion of pulmonary circulation → hypoxic vasoconstriction → decrease surfactant and release of inflammatory substances → pulmonary edema and atelectasis
- Symptoms:
- Increase dead space bc of areas that are being perfused but not nec taking part in exchange à VQ mismatch –> dec PaO2 etc, pulm infarction/HTN → decrease CO, systemic HTN → shock
- These are all possible depending on size of embolism & how quickly the person deteriorates
