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CCRN > PULMONARY > Flashcards

PULMONARY Flashcards

1
Q

normal ventilation is…

A

~4L/min

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2
Q

anything that affects heath of diaphragm (deconditioning, hypoxemia, acidosis, hypophosphatemia) will adversely affect what?

A

ventilation

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3
Q

PE results in…

A

increased alveolar dead space; clot in pulmonary circulation; no blood flow past alveoli in that area of pulmonary circulation

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4
Q

normal ventilation/perfusion ratio:

A

4L ventilation/min (V) / 5L perfusion/min (Q)
ideal lung unit = 0.8 ratio, normal V/Q ratio
FiO2 0.21

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5
Q

good/bad lung down and why?

A

good because we want the blood to perfuse the good lung; if bad lung is down, more blood will go to that lung but pt may become hypoxemic

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6
Q

what is a shunt? what is the treatment?

A

extreme V/Q mismatch; 100% FiO2 will NOT correct hypoxemia; EX: ARDS

give 100% O2, PEEP to increase alveolar recruitment and prevent alveolar collapse

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7
Q

a shunt is the movement of blood from where in the heart?

A

right to left side of heart without getting oxygenated; venous to arterial

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8
Q

what is the normal physiological shunt?

A

thebesian veins of heart empty into the left atrium; reason why normal O2 sat on RA is 95-99%, never 100%

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9
Q

what is an anatomic shunt?

A

VSD or ASD

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10
Q

what is a pathologic shunt?

A

ARDS - blood goes to lungs but does NOT get oxygenated –> refractory hypoxemia

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11
Q

what are the benefits of PEEP?

A

prevents expiratory pressure from returning to 0, keeps it (+)
decreases surface tension of alveoli, preventing atelectasis
increase alveolar recruitment
increases driving pressure, extends time of gas transfer, allow decrease in FiO2
adding PEEP will help hypoxemia and decrease FiO2

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12
Q

pt with severe sepsis/septic shock may have normal PaO2, SaO2, hgb, clear lungs, adequate ventilation, and oxygen delivery, and a lactate of 10. why?

A

lactic acidosis because oxygen utilization is affected by sepsis/septic shock and results in anaerobic metabolism

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13
Q

what clinical indications make hemoglobin “hold on” to oxygen molecules and causes a shift of the oxyhemoglobin dissociation curve to the left?

A

aLkaLosis
Low PaCO2
hypothermia (coLd)
low 2,3-DPG

SaO2 high but O2 stuck to hgb and tissues do not get needed O2 as readily

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14
Q

what clinical indications make hemoglobin “release” the oxygen more easily to the tissue and causes a shift of the oxyhemoglobin dissociation curve to the right?

A

acidosis
high PaCO2
fever
high 2,3-DPG

good for tissues; SaO2 low but O2 easily released to tissues

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15
Q

what is 2,3-DPG? and what do high/low levels indicate?

A

organic phosphate in RBCs that has the ability to alter the affinity of hgb for oxygen

high levels results in hgb more readily releasing O2 to tissues
low levels results in hgb holding on to O2, less O2 available to tissues

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16
Q

what are some causes of decreased 2,3-DPG?

A

multiple blood transfusions
hypophosphatemia
hypothyroidism

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17
Q

what are some causes of increased 2,3-DPG?

A

chronic hypoxemia (high altitudes, chronic HF)
anemia
hyperthyroidism

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18
Q

carboxyhemoglobin levels and symptoms

A 
0-5% normal
<15% often in smokers, truck drivers
15-40% HA, confusion
40-60% LOC, Cheyne-Stokes respirations
50-70% mortality
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19
Q

what is the treatment for carbon monoxide poisoning?

A

100% FiO2 until sx resolve and carboxyhemoglobin level is <10%
hyperbaric oxygen chamber if available within 30min

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20
Q

what is static compliance?

A

measurement of elastic properties of LUNG
normal is ~45-50ml/cm H2O
TV/plateau pressure (minus PEEP)

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21
Q

what is dynamic compliance?

A

measurement of elastic properties of AIRWAYS
normal is ~45-50ml/cm H2O
TV/peak inspiratory pressure (minus PEEP)

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22
Q

patients with pulmonary problems that involve mainly the lungs have a decrease in static compliance but dynamic compliance may also be decreased, why?

A

lung pressures may transmit up to the airways

i.e. ARDS

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23
Q

how would static and dynamic compliance be in a status asthmaticus patient?

A

static compliance would be normal

dynamic compliance would be low

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24
Q

what is anion gap?

A

difference between positive and negative anions

normal 5-15mEq/L

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25
Q

what are some problems associated with an increase in anion gap?

A 
Ketoacidosis
Uremia
Salicylate intoxication
Methanol
Alcoholic ketosis
Unmeasured osmoles: ethylene glycol, paraldehyde
Lactic acidosis: shock, hypoxemia
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26
Q

what are some problems associated with a normal anion gap?

A

saline infusion (hyperchloremic acidosis)TPN
diarrhea
ammonium chloride
ARF, sometimes chronic

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27
Q

respiratory failure is…

A

rapidly occurring inability of lungs to maintain adequate oxygenation of the blood with or without impairment of carbon dioxide elimination

ABG - PaO2 of 60mmHg or less, with or without elevation of PaCO2 to 50mmHg or more with pH <7.30

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28
Q

what problems can lead to type 1 hypoxemic respiratory failure?

A

PNA, ARDS, atelectasis, pulmonary edema, massive PE, interstitial fibrosis, asthma

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29
Q

what problems can lead to type 2 hypercapneic respiratory failure?

A

CNS depression r/t drugs (opiates, sedatives), increased ICP, COPD (including asthma), flail chest, ALS, Guillian-Barre syndrome, MS, myasthenia graves, SCI

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30
Q

what problems can lead to type 3 combined respiratory failure?

A

ARDS, asthma, COPD

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31
Q

what are some S/S of acute hypoxemic respiratory failure?

A

pulmonary - tachypnea, adventitious breath sounds, accessory muscle use
cardiac - tachyarrhythmias (initial), bradyarrhythmias (late), HTN/hypoTN, cyanosis
neuro - anxiety, agitation

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32
Q

what are some S/S of acute hypercapneic respiratory failure?

A

pulmonary - shallow breathing, bradypnea, BS clear or adventitious
neuro - progressive decreased LOC

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33
Q

CPAP (continuous positive airway pressure) is indicated for what type of patient?

A

patients with hypoxemic respiratory failure who have increased work of breathing i.e carcinogenic pulmonary edema
settings include FiO2 and 1 pressure setting in cm H2O pressure

34
Q

BiPAP (bilevel positive airway pressure) is indicated for what type of patient?

A

patients with hypoxemic and/or hypercapneic respiratory failure
settings include FiO2 and 2 pressure settings, the inspiratory pressure (IPAP) and expiratory pressure (EPAP)
IPAP assists ventilation and EPAP assists oxygenation

35
Q

what are some advantages of noninvasive ventilation?

A

buys time for medical tx to take effect, reduces WOB, decreases preload and after load, improves oxygenation, improves ventilation (BiPAP), reduces atelectasis, prevents intubation and resultant risks

36
Q

what are some contraindications for NIV?

A

hemodynamic instability or life-threatening arrhythmias,
copious secretions, high risk of aspiration, impaired mental status (unable to protect airway), suspected pneumothorax, inability to cooperate, life-threatening refractory hypoxemia

37
Q

what are some types of COPD? and what can be seen with airflow in these types?

A

emphysema, asthma, bronchitis

easier for air to enter pulmonary system than exit

38
Q

what are some physiologic consequences of COPD?

A

dynamic hyperinflation r/t too much air in lungs
air trapping and auto-PEEP
LOW expiratory flow rate
acute exacerbation –> V/Q mismatch r/t ventilation problem and an increase in PaCO2
may have chronic CO2 retention

39
Q

what are some signs of acute exacerbation of COPD?

A

worsening dyspnea, increase sputum purulence, increase in sputum volume, hypercapnia, hypoxemia

40
Q

management of acute exacerbation of COPD includes…

A
  • titrate FiO2 to PaO2 >60mmHg or SaO2 >90%; careful not to overcorrect
  • bronchodilators (inhaled short acting beta agonist SABA i.e. albuterol; inhaled anticholinergic)
  • corticosteroids
  • abx (with PNA)
  • mechanical ventilation (noninvasive/invasive) PRN
41
Q

what are some S/S of status asthmaticus?

A

dyspnea, tachypnea
cough, chest tightness
accessory muscle use
wheezing –> decreased BS –> absent BS –> OMINOUS
V/Q mismatch
flattened diaphragm on CXR (air trapping)
tachycardia, pulsus paradoxus >15mmHg (severe is 18mmHg)
anxiety –> decreased LOC
may have elevated WBC, eosinophils
peak flow rate <80% if predicted, <50% is severe
hx of previous intubations (higher mortality)

42
Q

what is stage 1 of status asthmaticus progression as seen on ABG?

A

normal PaO2, respiratory alkalosis (decreased PaCO2)

43
Q

what is stage 2 of status asthmaticus progression as seen on ABG?

A

mild hypoxemia, respiratory alkalosis (decreased PaCO2)

44
Q

what is stage 3 of status asthmaticus progression as seen on ABG?

A

worsening hypoxemia, normalization of pH and PaCO2

45
Q

what is stage 4 of status asthmaticus progression as seen on ABG?

A

severe hypoxemia, respiratory acidosis

46
Q

how would you manage status asthmaticus?

A

measure peak flow rate (PFR) - admit if PFR is 50-70%, ICU if PFR <50%
bronchodilator: short-acting beta-2 agonists (albuterol)
anticholinergics (atrovent)
corticosteroids (systemic)
oxygen, pulse ox
hydration to prevent thickened secretions
avoid sedatives
intubation if: respiratory acidosis, severe hypoxemia, silent chest, change in LOC
if intubated: sedate, avoid paralytics b/c in addition to steroids it will increase incidence of neuropathy

47
Q

how would you manage status asthmatics on ventilator?

A

use low rate to increase exhalation time
use low tidal volumes to prevent auto-PEEP
increase inspiration/expiration (I/E) ratio, often greater than 1;3-4, to allow time for optimal exhalation and prevent auto-PEEP

48
Q

what is a pulmonary embolism?

A

partial/complete obstruction of pulmonary capillary ed by a blood clot or other substance (fat, air, amniotic fluid, or foreign material with disruption of blood flow to an area of the lung

massive: >50% occlusion
submassive: <50% occlusion
80-90% result from DVT

49
Q

what are some types of PE?

A

VENOUS - DVT
FAT EMBOLI - LONG BONE, PELVIS
air emboli - surgery, IV lines
catheter embolization
RA/LA or RV embolus - a fib/flutter (LA leading to stroke more common
amniotic fluid (rare) amniocentesis, abrupt placenta, or abortion
tumor emboli - malignancy causes increase in thrombin
septic emboli - bacterial/viral

50
Q

what are some S/S of PE?

A

dyspnea, tachypnea, tachycardia, CP, right sided S3 or S4, anxiety, apprehension, cough, hemoptysis, crackles, syncope, PETECHIAE (FAT EMBOLI), low grade fever, respiratory alkalosis, INCREASED ALVEOLAR DEADSPACE

if massive: hypoxemia, hypotension, EKG changes (RBBB, right axis deviation on ECG, tall peaked P-waves in lead II, RV strain, ST elevation in V1-V2), cardiopulmonary arrest - PEA

51
Q

how would you diagnose PE?

A 
PULMONARY ANGIOGRAPHY (gold standard)
V/Q scan - not definitive 
high speed CT scan
D-dimer: if (+) means clot in body
venous doppler
52
Q

how can PE be prevented?

A

mechanical - TEDs, SCDs

Rx - low-molecular weight heparin (lovenox) DAILY, low dose unfractionated heparin TID

53
Q

how would you treat PE?

A

maintain airway, ventilation, oxygenation
fluids
anticoags - heparin (80units/kg IVP, then 18units/kg/hr drip), or low-molecular weight heparin (1mg/kg q12hrs), Coumadin ON FIRST TX DAY if able
fibrinolytic therapy FOR ALL PTS WITH HEMODYNAMIC COMPROMISE WITH LOW RISK FOR BLEEDING
maintain CO (inotropes, fluids)
analgesics
IVC filter for selected pts
may require long-term anticoags

54
Q

what is pulmonary hypertension?

A

MEAN pulmonary artery pressure >25mmHg at rest and PAOP <16mmHg at rest with secondary RHF

normal pulmonary artery mean pressure is ~20mmHg b/c RV normally pumps into a low-pressure system

PH results in RV failure, cor pulmonale

55
Q

what are some S/S of pulmonary HTN?

A

exertion dyspnea, lethargy, fatigue r/t inability to increase CO
progression to RV failure, CP, syncope with exertion, peripheral edema
passive hepatic congestion may cause anorexia and ab pain
Ortner’s syndrome - cough, hemoptysis, and hoarseness
systolic ejection murmur, increased intensity of pulmonic component of S2, diastolic pulmonic regurgitation murmur, right sided murmur, and gallops are augmented with inspiration
RV hypertrophy, elevated JVD, hepatomegaly, peripheral edema, ascites, and pleural effusion

56
Q

how would you treat pulmonary HTN?

A

treat underlying cause
consider diuretics, oxygen, anticoags, digoxin, exercise
dilators used (CCBs, phosphodiesterase-5 inhibitors Viagra/Cialis)
possible lung transplant (bilateral or heart-lung)
possible atrial septostomy (right to left shunt)

57
Q

what is pneumonia?

A

acute inflammation of the lung parenchyma caused y an infectious agent that can lead to alveolar consolidation
can be bacterial, viral, fungal, parasitic

58
Q

what are some S/S of PNA?

A

chills, diaphoresis, fever, malaise, dehydration
tachycardia, CP
confusion (esp elderly)
productive cough, accessory muscle use
over area of consolidation on chest: increased tactile fremitus, dull percussion, bronchial BS or diminished, bronchophony (louder/clearer), ego phony (“e” to “a”), whispered pectoriloquy (whisper head better with stethoscope)

59
Q

how is PNA diagnosed?

A

CXR - consolidation/diffuse patchy infiltrates
sputum cx with gram stain
blood cx
WBC - may be high, normal or low in immunocompromised/elderly
WBC differential: increased bands >10%
hypoxemia on ABG
thoracentesis for effusions

60
Q

how would you treat PNA?

A

GOOD LUNG DOWN
oxygenation and ventilation - titrate FiO2
bronchial hygiene, chest PT
NIV, or intubation/mechanical ventilation as needed
bronchoscopy (lavage PRN)
mobilize, clear secretions
identify organism
abx
hydration, manage fever/glucose, nutrition
prevention: smoking cessation, flu/PNA vaccine

61
Q

most aspirations occurs in the right lung. why?

A

right mainstream bronchus is shorter, wider, and at less of an angle

62
Q

what are some S/S of aspiration?

A 
acute respiratory distress
presence of gastric contents in oropharynx
tachycardia
hypoxemia
crackles
copious secretions due to alveolar edema
hypotension
63
Q

how would you manage aspiration?

A

place pt in slight Trendelenburg on right side
suction mouth and pharyngeal areas
bronchoscopy for large particles
O2, titrate prn
intubate, ventilation pen
monitor for onset of noncardiogenic pulmonary edema (ARDS)
monitor for hypotension

64
Q

ARDS or ALI is a syndrome caused by…

A

a variety of acute conditions that trigger an inflammatory response resulting in an increase in permeability of the pulmonary capillary membrane that allows a transudation of proteinaceous fluid into the interstitial and alveolar spaces

REFRACTORY HYPOXEMIA (100% FiO2 and hypoxemia is still present)
sunt is present so PEEP needs to be provided in order to increase alveolar recruitment and treat refractory hypoxemia
65
Q

What is ARDS?

A

acute onset with precipitating event
bilateral infiltrates consistent with pulmonary edema
PaO2/FiO2 =200mmHg, regardless of level of PEEP
PAOP =18mmHg
type II alveolar cells are damaged

66
Q

What is ALI?

A

acute onset with precipitating event
bilateral infiltrates consistent with pulmonary edema
PaO2/FiO2 btwn 201-300mmHg, regardless of level of PEEP
PAOP =18mmHg
less severe of a shunt than ARDS

67
Q

what is surfactant? what is its purpose?

A

phospholipid/lipoprotein produced by Type II alveolar cells
stabilizes alveoli, “keeps them open”
increases lung compliance
eases WOB
maintains functional residual capacity (FRC)

68
Q

what are some causes of ARDS/ALI from “direct” injury?

A

aspiration, PNA, pulmonary contusion, fat/air embolism, O2 toxicity, inhalation injury, drowning, trans thoracic radiation

69
Q

what are some causes of ARDS/ALI from “indirect” injury?

A

sepsis, shock, head injury, non-thoracic trauma, blood transfusion, pancreatitis, burns, heart bypass, DIC

70
Q

what are some early S/S of ARDS/ALI?

A

tachycardia, apprehension, restlessness, milk dyspnea, respiratory alkalosis, few crackles, isolated infiltrate or “ground glass” appearance on CXR, PaO2 ~60 on RA

71
Q

what are some late S/S of ARDS/ALI?

A

tachycardia, episodes of bradycardia, agitation, extreme dyspnea, respiratory and metabolic acidosis, crackles, wheezes, white out/bilateral infiltrates on CXR, PaO2 ~30 on RA

72
Q

what is the treatment for ARDS/ALI?

A
  • intubation with mechanical ventilation
  • PEEP, usually 15cm H2O or greater; monitor for barotrauma, decreased CO, treat hypotension
  • limit plateau pressure to 30cmH2O or less
  • limit TV to 4-6mL/kg –> “permissive hypercapnea” to prevent volutrauma; low TV will cause an increase in PaCO2 and a drop in pH
    NO STEROIDS
73
Q

what are some complications of ARDS/ALI?

A

multisystem organ failure (renal, GI, CNS), secondary infections, pulmonary embolus, ileum, skin breakdown, malnutrition, barotrauma: pneumothorax, SQ emphysema

74
Q

what are some types of pneumothorax?

A

TENSION (air unable to exit –> mediastinal shift), life threatening
spontaneous
traumatic (open, closed, iatrogenic r/t therapeutic/diagnostic)

75
Q

what are some S/S of spontaneous or traumatic pneumothorax?

A

dyspnea, tachypnea, CP (not all cases), unequal chest excursion, tracheal deviation (if present) TOWARD affected side, hypoxemia (if large), decreased/absent BS on affected side

76
Q

what are some S/S of tension pneumothorax?

A 
tracheal deviation AWAY from affected side
tachycardia
DISTENDED NECK VEINS
HYPOTENSION
LIFE THREATENING
77
Q

how would you treat pneumothorax?

A

if >20% - chest tube to reestablish neg. pleural pressure, supplemental O2, treat pain

if <20% - O2, monitor for lung re expansion

78
Q

what to check for in chest tube assessments/management

A
  • water seal chamber - tidaling with deep inspiration is normal, bubbling is NOT normal (air leak), avoid high airway pressures to avoid air leak
  • suction control chamber - gauge or water level determines amount of suction, NOT water suction source
  • clamp only when changing systems; clamping cuts of negative pressure water seal chamber, lung may re collapse
79
Q

ETT placement

A

waveform capnography is most accurate
cuff inflation to 20cmH20 pressure
should be 3-5cm ABOVE CARINA
ABGs within 20-30min to assess acid/base

80
Q

vent settings for ARDS patient?

A

plateau (static) pressure <30cm
low tidal volume 4-6ml/kg
high PEEP 15-20cm

81
Q

vent settings for asthma patient?

A 
provide short inspiratory time and long expiratory time
low rate
low tidal volume
high peak flow rate
monitor for auto-PEEP
82
Q

how to determine vent settings?

A
  • breath rate determined by PaCO2; 12-16/min usually
  • tidal volume determined by patient ideal weight and problem; generally 8-10ml/kg
  • FiO2 - set all 100% then titrate down according to PaO2; goal is to decrease to <50% asap

CCRN (10 decks)

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