Exam 2 Respiratory Flashcards
respiratory system
RS = Nose > pharynx > larynx > trachea > bronchi > bronchioles > lungs
Nose reaches blood vessels
Ex: winter time > dry nose > prone to nose bleeds
nose and blood vessels
Nose reaches blood vessels
Ex: winter time > dry nose > prone to nose bleeds
Inhale > moisten and warm the air > why it reaches blood vessel
volume of oxygen dissolved in the plasma
varies directly with the partial pressure of oxygen in the arteries
if the pressure of oxygen in the arterial blood (PO2) is within 90-100 mmHg, Hgb is maximally saturated with oxygen > tissues remain oxygenated
process of gas exchange
- Air enters to the alveolus on inspiration > air moves across the alveolar membrane > to the RBC
- At the same time > carbon dioxide moves from the RBC > to the alveolus > excreted during expiration
Summarized = Air we inhale goes to alveoli > air gets diffused into the capillaries > CO2 from capillaries gets diffused into the alveoli > gets exhaled
alveoli / Function
thin-walled/ballon-like structure surrounded by pulmonary capillaries
oxygen (now in the blood) combines with the heme (part of hemoglobin) to form oxyhemoglobin
from lungs and goes to L atrium > L ventricle > to rest of body
clinical implication: O2 saturation
oxygen saturation of hemoglobin (blood) is measured by pulse oximeter
O2 stat machine = use pulse oximeter
ex: nasal cannula > 92% RA w/ 2L NC
Perfusion
movement of blood through pulmonary circulation
ventilate in order to perfuse
diffusion
transfer of gases btw alveoli and pulmonary capillaries
V-Q ratio (ventilation-perfusion ratio)
ratio of air reaching alveoli to amount of blood reaching alveoli
V and Q are equal when they are both matching
shunt
Perfusion no ventilation
- blockage to prevent O2 from reaching blood
- ANY respiratory disorders can cause this (secretions or blockage) or anything that would restrict air from reaching
ex: pneuomnia, PE, Reduction of secretion - fluid in lungs/mucous - air present but cannot reach to area due to block
dead space
Vent no perfusion
no blood reaching area due to blockage
O2 reaches to the area but no blood flow
ex. Blood clot in pulm artery
V-Q mismatch (ventilation-perfusion ratio)
when air cannot flow into alveoli or blood flow is altered to alveoli
Ex. PE: blood clot preventing delivery of blood to complete gas exchange
airway obstruction: blocked and cannot pass through > less oxygen
Hypercapnia Normal “main” stimulus to breathing
pons and medulla = respiratory center
sensitive to high CO2 levels
hypoxic drive
Becomes the trigger for breathing
ex: case to individuals with COPD
chronic elevation of CO2
central receptors (pons in medulla) become less responsive to stimulus > allows peripheral chemoreceptors of low O2 to take over as stimulus of respiration (hypoxic drive)
peripheral chemoreceptors
located in common carotid artery
low O2
monitor O2 levels, more sensitivity
breathing changes when these receptors take over
“I don’t care if you wanna eat or not”
central receptors
high CO2
“Please eat!!”
In brain - pons and medulla (located near respiratory center in medulla)
baroreceptors (for BP)
located in aortic arch and carotid artery > can send signals to ANS depending on BP > if systolic BP drops > SNS is stimulated to increase HR and RR
ANS = SNS AND PNS
clinical: If BP is going down > HR will go up
- less blood to parts so body compensates to increase HR
- Breath faster to get more O2
dyspnea
perceived or feeling of shortness of breath or difficulty breathing
cough
prevents accumulation of secretions and and entry of irritating substances
defense mechanism of body to get rid of foreign substances in resp tract
cough expectorants
mucolytics, liquify secretions
use for AMs
cough suppressants
reduce cough
use for sleep or when infection not present
ex: lecturing > talking > take cough suppressants to solve (bc prob not due to infection)
hemoptysis
from lungs, coughing up sputum that contains blood
hematemesis
from GI, blood in vomit
atelectasis
collapse of alveoli
expose to pneumonia and affects perfusion
hypoxia
insufficient O2 levels
dead space and shunting can lead to hypoxia
pneumonia
inflammation of lung tissues
cap
- Used to describe infections from organisms found in the community rather than in the hospital or nursing home
- Infections that begins outside the hospital or is diagnosed within 48 hours after hospital admission to as person who has NOT resided in a long-term care facility for 14 days or more before admission
- Had prior entering hospital, dx within first 48hrs > covers hospital so cannot be blamed
- Most common CA = streptococcus pneumoniae
hap
hospital acquired pneumonia
- Pneumonia that was not present or was not incubating on admission to the hospital (occurring 48 hrs or more after admission)
- VAP - special type of HAP
- Most common cause = staphylococcus aureus particularly MRSA (methicillin-resistant SA)
- For VAP, in addition to MRSA, enterococcus is common like VRE (vancomycin-resistant enterococcus)
vap
ventilator associated pneumonia
pneumonia in immunocompromised person
common causes = s. aureus, aspergillus, candida
fungal related
aspiration pneumonia
- Accidental inhalation of substances
- Poor swallowing
- Reflux from stomach contents
- Comatose
- Must have patients in an elevated head position to reduce reflux (Cannot have patients fully supine = dangerous esp for older)
- Will be placed on special diet > speech consult (Recommend = thicken liquids, thin is harder to swallow)
typical pneumonia
bacterial pneumonia
cap, more inflammation and inflammatory response
atypical pneumonia
viral or nonbacterial penumonia
viral has less striking symptoms, more dangerous
pneumonia etiology
- Most common are bacteria and viruses
- Inhalation of chemicals
- Aspiration of oropharynx contents
- Accidentally inhales (saliva, mucous, etc)
- Infectious agents like fungi
pneumonia and flu
major risk factor
can alter pulmonary immune defenses (eventually lowering the resistance) > secondary pneumonia
pneumonia pathophysiology
cause > enters upper airways (inhale and reaches nose, pharynx, larynx) > reaches lungs and other parts of resp tract > CA adheres to respiratory epithelial cells (worse if a lot of secretions are there bc secretions are a good medium for CA/sticks well)»_space;>
- Stimulates inflammatory resp»_space; s/s of inflammation
- Resp cells try to produce mucous = attempt to counteract microorganisms in the hope that when you cough, you cough out the microorganism
- Resp cells are irritated by foreign substance»_space; cough
Mucus plus effect of inflammatory response > exudative fluids > accumulation in alveoli > crackles through stethoscope > alveoli are downed with secretions > SOB and s/s of hypoxia
restrictive and obstructive lung disorders
caused by conditions that limit expiratory airflow
ex: asthma, COPD, bronchiectasis
restrictive lung disorders are characterized by reduced lung expansion (lungs don’t expand properly)
ex: pulmonary fibrosis, thoracic cage deformities (kyphosis - quasimodo)
restrictive and obstructive lung disorders: hypercapnia causes
increase CO2 in blood
- PCO2 > 45 mmHg
- Usual cause = bradypnea (slow breathing)
- Other causes = asphyxiation, aspiration, pneumonia, pulmonary edema
chronic hypoxia
like hypoxemia = diminished level of O2 in the blood
COPD
chronic obstructive pulmonary disease
COPD related to chronic bronchitis, emphysema, chronic asthma
major cause of COPD
smoking
other genetic predisposition, IV drug users (develop comorbidity to lead to COPD), exposure to occupation dusts and chemicals
low level of O2
(remember - normally it is the increased level of CO2 that stimulates one to breathe)
CO2 levels is chronically high so it is LOW LEVEL OF O2 THAT STIMULATES
COPD manifestations (3)
- Absent during the early phase
- Dyspnea = usually first symptom
- Can easily be ignored (“I’m just tired”) - Cough or wheezing
- No respiratory infection but keep coughing = sign for COPD
COPD and chronic CO2
- CO2 chronically elevated so peripheral chemoreceptors take over to breath
- Give more O2 > remove hypoxic drive > cannot breath on own > sleepy or coma
- Worry about O2 stats?
a. Cannot breathe = give O2 (goal is to relieve SOB)
b. No s/s but low O2 state = can wait, depends on display of s/s
chronic bronchitis
definition, smoking leads to (2
inflammation of the bronchi persisting over a long time
smoking + recurrent respiratory infections > hypersecretion of mucus in large airways >
a) sputum over production
b) affectation of small airways (bronchioles)
chronic bronchitis and affectation of small airways (2)
affectation of small airways > increased mucus production > plugging of the airways > hypoxia >
a) cyanosis > “blue bloater”
- Cyanosis + generalized edema = “blue bloater”
b) stimulation of pulmonary arterial vasoconstriction
chronic bronchitis and stimulation of pulmonary arterial vasoconstriction
stimulation of pulmonary arterial vasoconstriction > increased resistance to pulmonary artery > affectation of the right ventricle > right ventricle hypertrophy
> > affectation of right atrium, then superior vena cava and inferior vena cava > congestion, edema > right ventricular heart failure (cor pulmonale)
pulmonary hypertension
increase pressure of pulmonary artery > affects R ventricle (hypertrophy) > back up of blood into R atrium > back up into SVC (traffic jam)
can be caused by chronic hypoxia
cor pulmonae
R ventricular failure due to pulmonary HTN there before chronic bronchitis/noncardiac heart failure (failure is in lungs)
emphysema
a condition in which the air sacs of the lungs are damaged and enlarged, causing breathlessness
Cause: smoking and inherited deficiency of alpha1-antitrypsin (makes lungs prone to injury)
alpha1-antitrypsin
anti protease enzyme, protects lungs from injury
emphysema and smoking
smoking >
a) attraction of inflammatory cells (cells in long) > release of elastase
- Normally alpha 1 antitrypsin prevent the release of elastase
b) diminishes α 1 antitrypsin activity (antitrypsin inhibits the release of elastase)
end result
elastase > destroys elastic fibers in the lungs > loss of lung elasticity (recoil) > alveoli become hyperinflated (permanently) > remain oxygenated (early stages) > person appears pinkish (bc more O2) > “pink puffer” (purse lip puffing)
hyperinflated alveoli
eventually they will burst/rupture and form air pocket (trapped) and can no longer complete exchange of gases
late stage of emphysema
patient may/can eventually develop cyanosis
