Respiratory Flashcards
phrenic nerve
c3-c5 innervates the diaphragm - receives involuntary and voluntary messages from the CNS
respiratory center - where is it located? parts?
located in the brainstem
- dorsal respiratory group: sets the basic automatic rhythm - detects CO2 and O2 levels in the arterial blood
- ventral respiratory group: contains inspiratory and expiratory neurons - becomes activated when increased ventilatory effort is necessary
- pneumotaxic and apneustic centers: located on the pons - modifiers of the inspiratory depth and rate that are established by the medullary centers
central chemoreceptors are stimulated by? what do they cause?
stimulated by H+ in CSF - low pH/acidosis - this reflects PaCO2
increase RR and depth
peripheral chemoreceptors located where? responsible for? do what?
located in the aorta and carotid bodies
stimulated by hypoxia PaO2
responsible for the increase in ventilation that occurs in response to arterial hypoxemia
normal V/Q ratio
4L/min ventilation; 5L/min perfusion - 4/5= 0.8
minute ventilation
RR x TV - normal is 6L
12x500 = 6000mL = 6L
acid-base balance formula
CO2 + H2O H2CO3 HCO3- + H+
carbonic anhydrase combines CO2 and H2O to form carbonic acid - carbonic acid dissociates into HCO3- and H+
How much venous CO2 is in bicarbonate form?
60%
*H+ binds to hgb and the HCO3- moves out of the RBC into the plasma
How much arterial CO2 is in bicarbonate form?
90%
*H+ binds to hgb and the HCO3- moves out of the RBC into the plasma
Principles of gas exchange - diffusion depends on?
partial pressure of gas
haldane effect?
Oxygenation of blood in the lungs displaces carbon dioxide from hgb which increases the removal of carbon dioxide. Consequently, oxygenated blood has a reduced affinity for CO2
determinants of arterial oxygenation
rate of oxygen transport to the tissues in the blood, and rate at which oxygen is used by the tissues
oxyhemoglobin shift to the left
shift up*
- hbg’s increased affinity for oxygen - promotes association in the lungs and inhibits dissociation in the tissues, low levels of 2,3 BPG
- alkalosis (high pH), hypocapnia, and hypothermia
oxyhemoglobin shift to the right
shift down*
- hbg’s decreased affinity for oxygen – increase in the ease with which oxyhemoglobin dissociates and oxygen moves into the cells
- happens when cells need more O2 - acidosis (low pH), hypercapnia, and hyperthermia, high levels 2,3 BPG
tidal volume
TV - volume of air inspired and expired with each normal breath around 500mL in normal male
inspiratory reserve volume
IRV - extra volume of air that can be inspired over and above the normal tidal volume when the person inspires with full force around 3000mL
expiratory reserve volume
ERV - max extra volume of air that can be expired by forceful expiration after the end of a normal tidal expiration around 1100mL
residual volume
RV - volume of air remaining in the lungs after the most forceful expiration around 1200mL
vital capacity
VC - amount of air exchanged from max inspiration to max expiration
Total lung capacity
total amount of air in the lung after forced inspiration
Kussmaul respirations
hyperpnea - increase volume of air during breathing
slightly increased ventilatory rate, very large tidal volume (deep breathing), no expiratory pause
Cheyne-Stokes respirations
occurs with what?
alternating periods of deep, shallow, apnea (15-60 seconds), followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea
*occurs with decreased brainstem blood flow
causes of hypoventilation, and results in?
causes respiratory acidosis and hypercapnia
O,RN
airway obstruction, chest wall restriction, altered neurologic control of breathing
causes of hyperventilation
anxiety, head injury, severe hypoxemia
HAH-perventilate
it’s considered hypercapnia at what level
PaCO2 > 44
causes of hypercapnia d/t hypoventilation and why does this occur?
occurs from decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation
causes: drugs, brainstem (medulla) injury, spinal cord injury, NMJ dysfunction, respiratory muscle dysfunction (myasthenia gravis), thoracic cage abnormalities, airway obstruction, sleep apnea
hypoxemia vs hypoxia
most common cause of hypoxemia
hypoxemia is decreased PaO2 in the blood; hypoxia is decreased O2 in the cells/reduced level of tissue oxygenation
Most common cause of hypoxemia: V/Q perfusion abnormalities
Shunting - what is it caused by?
shunting blood to areas that are better ventilated by using vasoconstriction
caused by very low V/Q ratio (could be due to too little ventilation or too much blood)
could be d/t atelectasis
most important cause: low alveolar partial pressure of oxygen; acidemia and inflammatory mediators
primary pneumothorax
spontaneous, occurs unexpectedly in healthy individuals
secondary pneumothorax
occurs d/t disease, trauma, injury, or condition
latrogenic pneumothorax
caused by medical treatments, especially needle aspiration/biopsies
Open pneumothorax
air pressure in pleural space equals barometric pressure b/c air that is drawn into the pleural space during inspiration is forced back out during expiration - air is not trapped
tension pneumothorax
s/s
site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration, but preventing its escape by closing up during expiration - air is trapped – life threatening
s/s: sudden pleural chest pain, tachypnea, possible mild dyspnea
*severe hypoxemia, tracheal deviation away from affected lung, hypotension (heart interference from pressure)
pleural effusion
presence of fluid in the pleural space
transexudative pleural effusion
watery and diffuses out of the capillaries
exudative pleural effusion
less watery and contains high concentrations of WBC’s and plasma proteins
chylothorax pleural effusion
chyle exudate from stomach contents
hemothorax pleural effusion
blood exudate
s/s of pleural effusion
dyspnea, pleural pain/chest pain
Pleuritic chest pain is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling. It is exacerbated by deep breathing, coughing, sneezing, or laughing. When pleuritic inflammation occurs near the diaphragm, pain can be referred to the neck or shoulder - pleurisy = lining of the lung becomes inflamed
empyema - what it is? s/s?
infected pleural effusion – pus in the pleural space
s/s: cyanosis, fever, tachycardia, cough, pleural pain
restrictive lung disease - what is it, and what are common causes?
In a restrictive lung disease, the compliance of the lung is
reduced, which increases the stiffness of the lung and limits
expansion. In these cases, a greater pressure (P) than normal is
required to give the same increase in volume (V).
Common causes
of decreased lung compliance are pulmonary fibrosis, pneumonia
and pulmonary edema.
*stiff lungs, stiff chest wall, WEAK muscles
FEP
obstructive lung disease
Difficult to get air out
In an obstructive lung disease, airway obstruction causes an
increase in resistance. During normal breathing, the pressure volume relationship is no different from in a normal lung. However, when breathing rapidly, greater pressure is needed to overcome the resistance to flow, and the volume of each breath gets smaller.
Common obstructive diseases include asthma, bronchitis, and emphysema.
- mechanical obstruction, increased resistance, increased tendency for airway closure
- remember that with obstructive lung diseases it’s harder to get air out b/c during expiration the airways narrow. So things that get in the way of the airway…
Changes in PFT for obstructed lung
decreased VC, IRV, ERV
increased RV, FRC, TLC
Changes in PFT for restrictive lung disease
decrease VC, RV, FRC, VT, TLC (all decreased)
typical s/s of restrictive lung diseases
cough, sputum, decreased lung volumes, hypoxemia, orthopnea, increased work of breathing, poor response to oxygen supplementation
typical s/s of obstructive lung diseases
increased WOB, V/Q mismatching, decreased forced expiratory volume in one second (FEV1), use of accessory muscles, expiratory wheezing, coughing, prolonged expiration, tachypnea, decreased exercise tolerance, SOB, tripod positioning, increased AP diameter
FEV1/FEV in obstructive and restrictive?
FEV1 - forced expiratory volume in 1 second
Obstructive disease; FEV1/FVC ratio decreased
• Restrictive disease; FEV1/FVC ratio can be normal;
or increased
more examples of restrictive lung diseases
aspiration (mostly R), atelectasis, pulmonary fibrosis, O2 toxicity, pneumoconiosis (inhaled dust changes lungs)
s/s of asthma
chest constriction, expiratory wheeze, dyspnea, nonproductive cough, prolonged expiration, tachycardia, tachypnea
pulsus paradoxus: decreased systolic pressure >10mmHg during inspiration
Status asthmaticus: not reversed by usual measures - life threatening
*ominous signs of impending death: silent chest, PaCO2 > 70
chronic bronchitis
hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year for at least 2 consecutive years
inspired irritants increase mucous production, size and number of mucus glands, and bronchial edema – thick mucus compromised lungs defenses
hypertrophied bronchial smooth muscle
s/s bronchitis
decreased exercise tolerance, wheezing and SOB, copious productive cough, polycythemia from chronic hypoxemia, decreased FEV1, increased infections
acute bronchitis - cause and s/s?
acute infection or inflammation of airways of bronchi commonly following viral illness
symptoms are similar to pneumonia but no consolidation or chest infiltrates – nonproductive cough occurs in paroxysms and is aggravated by cold, dry, dusty air
Emphysema - loss of what? destruction d/t?
loss of elastic recoil
destruction of the alveoli occurs through the breakdown of elastin in the septa as a result of an imbalance b/w proteases and anti-proteases, oxidative stress, and apoptosis – also produces larges air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs)
types of emphysema
centriacinar (centrilobular): septal destruction occurs in the respiratory bronchioles and alveolar ducts; upper lobes
panacinar (panlobular): involves the entire acinus; damage is more randomly distributed; involves lower lobes
primary emphysema caused by
inherited deficiency of the enzyme a1-antitrypsin
secondary emphysema caused by
cigarette smoking, air pollution, occupational exposures, and childhood respiratory infections
CF chronic inflammation leads to…
chronic inflammation leads to hyperplasia of goblet cells, bronchiectasis, pneumonia, hypoxia, fibrosis, etc.
pulmonary HTN causes?
Active constriction of the vascular bed caused by?
elevated left ventricular pressure, increased blood flow through the pulmonary circulation, obliteration or obstruction of the vascular bed, active constriction of the vascular bed produced by hypoxemia or acidosis
patho of pulmonary HTN
overproduction of vasoconstrictors (thromboxane) and decreased production of vasodilators (NO, prostacyclin),
remodeling of pulmonary artery intima, resistance to pulmonary artery blood flow increasing the pressure in the pulmonary arteries; workload of the right ventricle increased and subsequent right ventricular hypertrophy – may be followed by failure and eventually death
Cor pulmonale
secondary to PAH - pulmonary HTN creating chronic pressure overload in the right ventricle
most frequent cause of cancer death in the US
lung cancer d/t cigarette smoking
Laryngeal bronchogenic caner
risk factors? s/s?
smoking, worse smoke + etoh, GERD, HPV
s/s: progressive hoarseness, dyspnea, cough
NSCLC - 3 types
85% of lung cancers
squamous cell carcinoma: nonproductive cough or hemoptysis
adenocarcinoma: tumor arising from glands - asymptomatic or pleuritic chest pain and SOB
large cell carcinoma: chest wall pain, pleural effusion, cough, sputum, hemoptysis, airway obstruction –> pneumonia
SCLC - arise from?
neuroendocrine
10-15 % of all lung cancers
worst prognosis – rapid growth and early metastasis
strongest correlation with smoking
arise from neuroendocrine tissue – ectopic hormone secretion – paraneoplastic syndromes (hyponatremia ADH, cushing syndrome - ACTH, hypocalcemia - calcitonin, gynecomastia - gonadotropins, carcinoid syndrome - serotonin)
lung carcinoid tumor - rate of growth? spread?
5% of all lung cancers
grow slowly and rarely spread
absorption atelectasis
gradual absorption of air from obstructed or hypo-ventilated alveoli
compression atelectasis
external compression on the lung
surfactant impairment atelectasis
decreased production or inactivation of surfactant
most common cause of pulmonary edema?
left sided HF - caused by increase in capillary hydrostatic pressure
post-obstructive pulmonary edema caused by
rare, life-threatening complication that can occur after relief of upper airway obstruction – obstruction causes negative pressure to build and build as breathing attempts occur
s/s of pulmonary edema
dyspnea, orthopnea, hypoxemia, SOB, pink frothy sputum
ARDS clinical manifestation progression
dyspnea and hypoxemia with poor response to oxygen supplementation – hyperventilation and respiratory alkalosis – decreased tissue perfusion, metabolic acidosis, organ dysfunction – increased WOB, decreased TV, and hypoventilation – hypercapnia, respiratory acidosis, worsening hypoxia – decreased cardiac output, hypotension, death
virchow’s triad
venous stasis, hypercoagulable state, injury to endothelial cells
pulmonary embolism results in
results in widespread hypoxic vasoconstriction, decreased surfactant, release of neurohumoral substances, atelectasis of affected lung segments further contributing to hypoxemia, pulmonary edema, pulmonary HTN, shock, and even death
