Pathophysiology Flashcards
You need to excrete ________ to bring PH levels down
Bicarbonate (CO2)
CNS depressing drugs can potentially cause..
Respiratory acidosis
-hypoventilation
-not enough bicarbonate being excreted through breathing
PH under __________ is acidosis
Under 7.35
Normal: 7.35-7.4
If a patient is compensating for respiratory acidosis, what will be high?
HCO3-
(this is a akaline substance and it helps make the PH less acidic).
Respiratory acidosis will lead to
______cardia
confusion
headache
reslessness
Tachycardia
__________ventilation will cause respiratory alkalosis
Hyperventilation
Drugs that stimulate the respiratory system can cause…
Respiratory alkalosis
Note: can also be caused by anxiety, pain, fever, or **sepsis **
Hyperventilation leads to ______
Hypoventilation leads to ________
Hyper- alkalosis
Hypo- acidosis
A patient has respiratory alkalosis if PH is above
7.45
Rapid deep breathing, parasthesia, light headedness, anxiety
are symptoms of
respiratory alkalosis
Diuretics/Renal Disease (too much excretion)
Vomiting/Diarrhea (Loss of hydrochloric acid)
Or decreased plasma potassium levels
These often cause …..
Metabolic Acidosis
Please note that **low hydrogren levels often follow low potassium levels **
If someone has metabolic acidosis, what are they retaining too much of?
CO2
If someone is compensating for metabolic alkalosis, what will you see?
Higher PaCO2 in order to try to make the blood more acidic
Slow, Shallow breathing
Confusion
Hypertonic muscles
restlessness
seizure
These are signs of
Metabolic alkalosis
Note: You’re breathing slow and shallow to retain CO2
Hyperkalemia
Liver disease can cause excess HCL acid, this could lead to…
Metabolic Acidosis
Note that H+ Follows potassium!
Uncontrolled diabetes -> Hyperglycemia -> Ketone bodies
These cause ___________
Metabolic acidosis
Kussmal’s Respiration is often seen with ____________
Metabolic acidosis
Rapid Deep breathing in an attempt to excrete CO2 and bring PH back to normal
What are signs of diabetic ketoacidosis
Excess Thirst
Urination
Fruity Breath
Drowsiness
When looking at patient stats
HCO3 represents the __________ system
Whereas CO2 represents the ________ system
Metabolic system
Respiratory system
Patient 1:
PH 7.55 (high PH)
CO2 = 32 (Low)
HCO3 = 20 (Low)
What is the problem?
Respiratory alkalosis
w/ partial compensation (partial because PH is not back to normal, but HCO3 is low)
PH 7.47 (High)
PaCO2: 61 (High)
HCO3: 43 (High)
What is the problem?
Metabolic alkalosis w/ partial compensation
PH 7.26 (Low)
PaCO2 (High)
HCO3 (Normal)
What is the problem?
Respiratory acidosis w/ no compensation
If vital capacity is under 80% of what is predicted, then you have a _______ lung disorder
restrictive
-cannot inhale
If vital capacity is over 120% what is predicted you have a ________ lung disorder
obstructive
-cannot exhale
Obstructive patients tend to have a _______ lung with ________ FVC1
Large
Less
Asthma
Chronic Bronchitis
Emphysema
Cystic Fibrosis
These are all examples of
Obstructive disorders
T or F, an obstructive lung patient will have increased Residual Lung Volume
T
T or F, an obstructive lung patient will have increased Inspiratory and Expiratory reserve volume
False, these decrease
What is FEV1?
What is FVC?
FEV1 = forced amount of air out of lung in 1 sec
FVC= Forced vital capacity = How much air you can exhale TOTAL
If FEV1/FVC is under _______, you’ve got obstrutive lung disease
70%
How does chronic bronchitis obstruct the lung?
Inflamed airways cause excessive mucus production → prevents exhalation and trap air
How does emphysema obstruct the lung?
destruction of terminal bronchioles/alveolar walls → stretched out alveoli → reduces SA for O2 diffusion → increase CO2, decrease O2
Alveoli become less efficient at gas exchange (destruction of alveioli wall) and trap air
What are the 2 types of COPD?
Chronic Bronchitis and emphysema
Emphysema causes ____________ lung tissue compliace
Increased
What is better for COPD patient’s, huffing or coughing?
Huffing
Productive cough on most days for 3 months during 2 consecutive years is the diagnositc criteria for ___________
Chronic bronchitis
GOLDS GRADES AND SEVERITY OF AIRWAY OBSTRUCTION IN COPD
Mild- above 80% predicted FEV1 (normal)
Moderate 80-50
Severe 50-30
Very Severe 30 and under
at what GOLD grades due PT’s work with patients?
GOLD 2 and 3
-these patients are symptomatic (SOB and accessory muscle usage)
What is predicted FEV1 based on?
Race, weight, height, Gender….
COPD Assessment Test
asks about coughing, mucus production, breathlessness, sleep, and energy level
-use for baseline/goals
Emphysema patients ___________ oxygen desaturation during exercise
Chronic bronchitis patients ____________ oxygen desaturation during exercise
Develop
MAY DEVELOP (W/ chronic bronchitis sometimes the exercise helps them clear the secretions)
At the beginning of Emphysema, their SPO2 is normal at rest, why?
Because they’re able to compensate by breathing faster (requires more energy)
Exercise will make SPO2 drop when they cant keep up w/ demand ‘
THIS IS WHY PACED BREATHING IS IMPORTANT FOR EMPHYSEMA
at what SpO2 should you be concerned for COPD patients
usually if it drops below low 80s (they live at 88%)
*important to consult with physician
Two kinds of Emphysema:
Panacinar
Centrilobublar
panacinar emphysema
Affects alveoli, affects whole lung, primarily lower lobes, genetic predisposition
centrilolbar emphysema
most common type due to smoking, affects respiratory bronchioles, primary upper lobes
What is a Bullae?
Hypercompliant “balloon” structure in lung seen in emphysema
Emphysema patients might have a ___________ chest deformity causing a ______ diaphram
barrel chest
flatter
Emphysema patient’s have a increased residual volume and an increased ____________
Functional residual volume - (basically Residual volume + expiratory reserve volume)
Emphysema patients have ___________ breath sounds
DECREASED bilaterally
(too much air, sound doesn’t travel well!)
How does emphysema lead to R sided Heart Failure
Low oxygen ->
Pulmonary artery constriction (to try to balance V/Q ratio) ->
Pulmonary hypertension ->
Too much work for R side of heart
Why are emphysema patient’s more prone to clots and pulmonary embolism?
Relative increase in hematocrit because less oxygen in blood = more RBC = Thicker blood
Why is there increased risk of nocturnal death w/ emphysema
Less ventilation overall during REM sleep leads to cardiac arrythmia
On a patient w/ emphysema, what will you see on their chest xray
More ribs = hyperinflated
5-7 is normal
7+
(I think these numbers are talking about how many ribs you can see covering the lung, more ribs = bigger lung)
Why is pursed lip breathing important for obstructive patients?
Maintain positive airway pressure in lungs to prevent collapse upon rapid exhalation
Why do chronic bronchitis patients have excessive mucus
Goblet and mucoid cell hyperplasia
Reduced cillary activity
Frequent infections
chronic bronchitis and polycythemia
too many red blood cells (RBCs) in your bloodstream. This increases your hematocrit and hemoglobin levels, which can thicken the blood which increases the workload on the heart
Who develops hypoxemia sooner, emphysema patients or chronic bronchitis patients
Chronic bronchitis
Chronic bronchitis leads to __________ which leads to R sided heart failure/cor pulmonale
Pulmonary hypertension
Why are chronic bronchitis patients blue
Cyanosis due to hypoxemia
asthma
obstructive lung disease: bronchospasm and airway narrowing due to increased responsiveness to chemical/environmental irritants
status asthmaticus
acute exacerbation of asthma → respiratory failure/death
causes of obstruction in asthma
bronchospasm
increased bronchial wall thickness
recurrent bronchial wall remodeling
hyper inflated lungs
early-mild exacerbations versus respiratory arrest asthma
early: wheezing
onset of respiratory arrest → wheezing stops
What will you hear often w/ asthma patients (more on expiration)
wheezing
extrinsic versus intrinsic asthma triggers
extrinsic: allergens
intrinsic: not associated with allergens
exercise induced asthma
mediated by water and/or heat loss from the airway
How is asthma treated?
Corticosteroids
Or medications that activate sympathetic NS and supress parasymp NS
Reversability of asthma w/ ____________ is greater than other obstructive lung diseases
Bronchodilators
What is the key to diagnosing asthma?
When they take a bronchodilator you see a 12% increase in FEV1
bronchiectasis
dilation of bronchial walls as a result of recurrent infections (retaining secretions)→ scar tissue weakens walls and walls are stretched by coughing
primary treatment for bronchiectasis
bronchial hygiene to remove secretions
3 types of bronchiectasis
cylindrical
varicose
saccular
restrictive disorders lung volumes
cannot inhale → DECREASED VC, RV, FRC, VT, TLC → small lung
effect of decreased lung compliance in restrictive lung diseases
decreased lung compliance → increased stiffness of lung → limits expansion → a greater pressure is required to give the same increase in lung volume
when breathing rapidly, greater pressure is needed to overcome the resistance to flow, resulting in
the volume of each breath gets smaller
*increase RR → increase resistance
acute pulmonary disorders examples
atelectasis
pneuomothorax
pneumonias
ARDS
chronic pulmonary disorders examples
bronchopulmonary dysplasia
pulmonary fibrosis
SLE
scleroderma
occupational lung diseases
lung carcinomas
bronchopulmonary dysplasia
lungs are not fully developed → lack surfactant
extra pulmonary restrictive disorders
fractures
kyphosis
scoliosis
rheumatoid arthritis
ankylosing spondylitis
neuromuscular disorders
pleural effusion
abdominal ascites
intrathoracic surgical implants
atelectasis
partial collapse of lung parenchyma (alveoli)
microatelectasis
alveolar collapse related to surface tension changes
what can cause microatelectasis
laying on side for too long → lung blocked from expansion → decreased ventilation
low mechanical pressure (PEEP)
signs of microatelectasis
discontinuous crackles
bronchial sounds (consolidation)
tracheal deviation
obstructive/regional atelectasis
bronchus becomes occluded (mucus) → air distal to obstruction is absorbed → lung region collapses
what side does a tracheal shift occur?
towards the side of atelectasis
bronchial pneumonia
OBSTRUCTIVE
- caused by staple/streptococcal
- LITTLE consolidation → patchy infiltrates on x-ray
-INCREASED MUCUS PRODUCTION → productive cough (purulent sputum)
lobar pneumonia
RESTRICTIVE
-CONSOLIDATION of parenchyma → hepatization
-PAINFUL
-dry cough
hepatization
Hepatization is a pathological term used to describe the solidification of lung tissue that normally is soft and air-filled—making it feel and look like liver tissue
three phases of ARDS
exudative
proliferative
fibrotic
exudative phases
produces leakage of water, protein, and inflammatory and red blood cells into interstitum and alveolar lumen
damage to type 1 and type 2 alveolar cells
result of damage to type 1 alveolar cells
irreversible damage → decreased respiration
result of damage to type 2 alveolar cells
impaired surfactant production (restrictive problem) → increase lung surface tension → lung collapse
proliferative phase
type 2 cells proliferate
fibrotic phase
irreversible fibrotic phase
collagen deposition in alveolar, vascular, and interstitial beds → increases distance of capillary alveolar membrane
ARDS clinical presentation
dyspnea
tachypnea
decreased lung compliance
hypoxemia
why are ARDS patients sedated?
to decrease the demand on the lung
emphysema alveoli characteristics
destruction of alveolar walls and half of the total available number of capillaries
restrictive disease alveoli characteristics
obstruction of alveolar duct and decreased area for gas exchange
PE alveoli characteristics
obstruction of the pulmonary circulation; no alvrolocapillary blood flow
alveoli characteristics during exercise
increase in number of open capillaries
mitral stenosis alveoli characteristic
capillary enlargement
ARDS alveoli characteristics
longer paths for diffusion due to thickening of alveolar epithelium
fibrotic alveoli characteristics
longer paths for diffusion due to tissue separating alveolar capillary from alveolar epithelium
pulmonary edema alveoli characteristics
longer paths for diffusion due to non ventilated alveoli filled with edema fluid or exudate
