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Advanced Patho UC > Respiratory > Flashcards

Respiratory Flashcards

1
Q

phrenic nerve

A

c3-c5 innervates the diaphragm - receives involuntary and voluntary messages from the CNS

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2
Q

respiratory center - where is it located? parts?

A

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
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3
Q

central chemoreceptors are stimulated by? what do they cause?

A

stimulated by H+ in CSF - low pH/acidosis - this reflects PaCO2

increase RR and depth

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4
Q

peripheral chemoreceptors located where? responsible for? do what?

A

located in the aorta and carotid bodies

stimulated by hypoxia PaO2

responsible for the increase in ventilation that occurs in response to arterial hypoxemia

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5
Q

normal V/Q ratio

A

4L/min ventilation; 5L/min perfusion - 4/5= 0.8

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6
Q

minute ventilation

A

RR x TV - normal is 6L

12x500 = 6000mL = 6L

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7
Q

acid-base balance formula

A

CO2 + H2O H2CO3 HCO3- + H+

carbonic anhydrase combines CO2 and H2O to form carbonic acid - carbonic acid dissociates into HCO3- and H+

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8
Q

How much venous CO2 is in bicarbonate form?

A

60%

*H+ binds to hgb and the HCO3- moves out of the RBC into the plasma

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9
Q

How much arterial CO2 is in bicarbonate form?

A

90%

*H+ binds to hgb and the HCO3- moves out of the RBC into the plasma

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10
Q

Principles of gas exchange - diffusion depends on?

A

partial pressure of gas

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11
Q

haldane effect?

A

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

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12
Q

determinants of arterial oxygenation

A

rate of oxygen transport to the tissues in the blood, and rate at which oxygen is used by the tissues

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13
Q

oxyhemoglobin shift to the left

A

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
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14
Q

oxyhemoglobin shift to the right

A

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
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15
Q

tidal volume

A

TV - volume of air inspired and expired with each normal breath around 500mL in normal male

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16
Q

inspiratory reserve volume

A

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

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17
Q

expiratory reserve volume

A

ERV - max extra volume of air that can be expired by forceful expiration after the end of a normal tidal expiration around 1100mL

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18
Q

residual volume

A

RV - volume of air remaining in the lungs after the most forceful expiration around 1200mL

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19
Q

vital capacity

A

VC - amount of air exchanged from max inspiration to max expiration

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20
Q

Total lung capacity

A

total amount of air in the lung after forced inspiration

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21
Q

Kussmaul respirations

A

hyperpnea - increase volume of air during breathing

slightly increased ventilatory rate, very large tidal volume (deep breathing), no expiratory pause

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22
Q

Cheyne-Stokes respirations

occurs with what?

A

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

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23
Q

causes of hypoventilation, and results in?

A

causes respiratory acidosis and hypercapnia

O,RN

airway obstruction, chest wall restriction, altered neurologic control of breathing

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24
Q

causes of hyperventilation

A

anxiety, head injury, severe hypoxemia

HAH-perventilate

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25
Q

it’s considered hypercapnia at what level

A

PaCO2 > 44

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26
Q

causes of hypercapnia d/t hypoventilation and why does this occur?

A

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

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27
Q

hypoxemia vs hypoxia

most common cause of hypoxemia

A

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

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28
Q

Shunting - what is it caused by?

A

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

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29
Q

primary pneumothorax

A

spontaneous, occurs unexpectedly in healthy individuals

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30
Q

secondary pneumothorax

A

occurs d/t disease, trauma, injury, or condition

31
Q

latrogenic pneumothorax

A

caused by medical treatments, especially needle aspiration/biopsies

32
Q

Open pneumothorax

A

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

33
Q

tension pneumothorax

s/s

A

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)

34
Q

pleural effusion

A

presence of fluid in the pleural space

35
Q

transexudative pleural effusion

A

watery and diffuses out of the capillaries

36
Q

exudative pleural effusion

A

less watery and contains high concentrations of WBC’s and plasma proteins

37
Q

chylothorax pleural effusion

A

chyle exudate from stomach contents

38
Q

hemothorax pleural effusion

A

blood exudate

39
Q

s/s of pleural effusion

A

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

40
Q

empyema - what it is? s/s?

A

infected pleural effusion – pus in the pleural space

s/s: cyanosis, fever, tachycardia, cough, pleural pain

41
Q

restrictive lung disease - what is it, and what are common causes?

A

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

42
Q

obstructive lung disease

A

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…
43
Q

Changes in PFT for obstructed lung

A

decreased VC, IRV, ERV

increased RV, FRC, TLC

44
Q

Changes in PFT for restrictive lung disease

A

decrease VC, RV, FRC, VT, TLC (all decreased)

45
Q

typical s/s of restrictive lung diseases

A

cough, sputum, decreased lung volumes, hypoxemia, orthopnea, increased work of breathing, poor response to oxygen supplementation

46
Q

typical s/s of obstructive lung diseases

A

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

47
Q

FEV1/FEV in obstructive and restrictive?

FEV1 - forced expiratory volume in 1 second

A

Obstructive disease; FEV1/FVC ratio decreased

• Restrictive disease; FEV1/FVC ratio can be normal;
or increased

48
Q

more examples of restrictive lung diseases

A

aspiration (mostly R), atelectasis, pulmonary fibrosis, O2 toxicity, pneumoconiosis (inhaled dust changes lungs)

49
Q

s/s of asthma

A

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

50
Q

chronic bronchitis

A

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

51
Q

s/s bronchitis

A

decreased exercise tolerance, wheezing and SOB, copious productive cough, polycythemia from chronic hypoxemia, decreased FEV1, increased infections

52
Q

acute bronchitis - cause and s/s?

A

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

53
Q

Emphysema - loss of what? destruction d/t?

A

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)

54
Q

types of emphysema

A

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

55
Q

primary emphysema caused by

A

inherited deficiency of the enzyme a1-antitrypsin

56
Q

secondary emphysema caused by

A

cigarette smoking, air pollution, occupational exposures, and childhood respiratory infections

57
Q

CF chronic inflammation leads to…

A

chronic inflammation leads to hyperplasia of goblet cells, bronchiectasis, pneumonia, hypoxia, fibrosis, etc.

58
Q

pulmonary HTN causes?

Active constriction of the vascular bed caused by?

A

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

59
Q

patho of pulmonary HTN

A

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

60
Q

Cor pulmonale

A

secondary to PAH - pulmonary HTN creating chronic pressure overload in the right ventricle

61
Q

most frequent cause of cancer death in the US

A

lung cancer d/t cigarette smoking

62
Q

Laryngeal bronchogenic caner

risk factors? s/s?

A

smoking, worse smoke + etoh, GERD, HPV

s/s: progressive hoarseness, dyspnea, cough

63
Q

NSCLC - 3 types

A

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

64
Q

SCLC - arise from?

A

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)

65
Q

lung carcinoid tumor - rate of growth? spread?

A

5% of all lung cancers

grow slowly and rarely spread

66
Q

absorption atelectasis

A

gradual absorption of air from obstructed or hypo-ventilated alveoli

67
Q

compression atelectasis

A

external compression on the lung

68
Q

surfactant impairment atelectasis

A

decreased production or inactivation of surfactant

69
Q

most common cause of pulmonary edema?

A

left sided HF - caused by increase in capillary hydrostatic pressure

70
Q

post-obstructive pulmonary edema caused by

A

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

71
Q

s/s of pulmonary edema

A

dyspnea, orthopnea, hypoxemia, SOB, pink frothy sputum

72
Q

ARDS clinical manifestation progression

A

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

73
Q

virchow’s triad

A

venous stasis, hypercoagulable state, injury to endothelial cells

74
Q

pulmonary embolism results in

A

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

Advanced Patho UC (14 decks)

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