Exam 2 Respiratory Flashcards
(97 cards)
1
Q
What is a VQ mismatch?
A
A ventillation and perfusion mismatch
Either part of the lung receives oxygen with no blood flow, or blood flow with no oxygen
Occurs when there is an obstruction either in the airway (choking) or blood vessel (Clot)
2
Q
What causes a VQ mismatch that effects perfusion?
A
pulmonary embolism
pulmonary hypertension
3
Q
What causes a VQ mismatch that effects ventillation?
A
pulmonary edema
airway obstruction
asthma
COPD
cystic fibrosis
lung mass
pneumonia
4
Q
What is the function of the alveoli?
A
site of gas exchange
surfactant keeps them open
large surface area
5
Q
What is the difference between pulmonary artery and pulmonary vein?
A
pulmonary artery carries deoxygenated blood
pulmonary vein carries oxygenated blood
6
Q
Pulmonary Artery
A
Most deoxygenated blood in the body
pulmonary artery pressure is lower than systemic
7
Q
hypoxia vs hypoexmia
A
hypoxia is low O2 in the tissue
hypoxemia is low o2 in the blood
8
Q
Respiratory diagnostic tests
A
radiology: CXR, V/Q scan, pulmonary angiography, CT scan, MRI
pulmonary function tests: PEFR, incentive spirometry
bronchoscopy: visualization, biopsy, lavage
Thorocentesis: intervention and test
ABG
9
Q
pH normal range
A
7.35 - 7.45
> 7.45 = alkalotic
<7.35 = acidic
10
Q
CO2 normal range
A
35-45 (acid)
11
Q
HCO3 normal range
A
22-28 (base)
12
Q
Alkalosis
A
pH > 7.45
too much base (HCO3)
too little acid (CO2)
13
Q
Acidosis
A
pH < 7.35
too much acid
too little base
14
Q
What happens if the respirations are too low?
A
carbon dioxide can’t leave the plasma and CO2 builds up
there will be an INCREASE in CO2 = more acidic blood = pH decreases
respiratory acidosis
15
Q
What causes respiratory acidosis?
A
asthma, COPD, pneumonia
16
Q
What happens if respirations are too high?
A
carbon dioxide leaves the plasma and is exhaled
there will be a DECREASE in CO2 = less acid in blood = pH increases
respiratory alkalosis
17
Q
What causes respiratory alkalosis?
A
anxiety, pulmonary embolism, fever
18
Q
What happens if there is a metabolic problem?
A
The body is creating too much acid or base, so the lungs will try and compensate by reataining or blowing off CO2
19
Q
metabolic acidosis causes
A
shock, lactic acidosis, DKA, diarrhea
20
Q
metabolic alkalosis causes
A
vomiting, diuretic use
21
Q
uncompensated ABG
A
opposite system has not attempted to compensate and remains normal
22
Q
partially compensated ABG
A
opposite system is outside normal range to try and compensate, but pH is still abnormal
23
Q
compensated ABG
A
opposite system is outside normal range in an effort to compensate, pH is normal
24
Q
how to tell if a problem is respiratory or metabolic?
A
ROME
respiratory opposite - arrows go opposite directions for pH and CO2
metabolic equal - arrows go the same direction for pH and HCO3
25
hypoxemic patient
paO2 low (<60) while receiving FiO2 of 60%
26
hypercapnic patient
paCO2 >45 with acidemia (pH <7.35)
27
acute respiratory failure
patient will either be hypoxemic or hypercapnic or mixed
28
Acute Respiratory Failure S&S
tachypnea
deep respirations (acidosis)
use of accessory muscles
dysrhythmias
confusion/restless
29
Acute respiratory failure collaborative care
treat underlying cause and reverse the 3 areas of compromise
1. treat underlying pulmonary problem
2. treat anxiety and restlessness
3. oxygenation
4. correct acidosis
5. mobilization of secretions
6. nutritional therapy
30
How to treat underlying pulmonary congestion?
diuretics
vasodilators
antihypertensives
31
How to treat pulmonary infection?
antibiotics
32
How to treat pulmonary inflammation
corticosteroids
33
How to treat bronchospasm?
bronchodilators, aerosol treatments
34
how to treat anxiety and restlessness?
correct CO2/O2 problem
low dose anxiety medication
35
How to correct acidosis?
hyperventilate
bicarb drip
36
acute respiratory failure nutritional therapy
high caloric and high protein
caution!* NG feedings while on CPAP/BIPAP
37
high flow nasal cannula
7-15 L/min
38
airvo
up to 100% fio2 at 60L/min
39
CPAP vs BiPAP
CPAP decreases work of breathing on inspiration
BIPAP is pressure on inspiration and expiration - better for COPD. Can help repell trapped CO2
40
Criteria for CPAP and BIPAP
1. patient must be able to protect their airway (gag/cough intact, patent, can swallow, low aspiration risk, low secretions)
2. Will the disease process likely to improve within the next 48-72 hours?
41
What type of patient will benefit from CPAP/BIPAP?
acute respiratory failure (hypercapnia)
COPD
cardiogenic pulmonary edema
option for DNI patietns
42
advantages of CPAP/BIPAP
non-invasive
decreased r/o pneumonia
no tracheal damage
no sedation
can be easilly removed and reapplied
can be used in non ICU setting
43
mechanical ventilation
improve tissue O2 that cannot be maintained by other forms of O2 therapy
requires intubation
44
tracheostomy complications
tracheal wall necrosis
tracheal dilation
tracheal stenosis
fistula formation
airway obstruction
infection
accidental decannulation
subcutaneous emphysema
45
What is PEEP
positive end expiratory pressure - keeps airways open between breaths to reduce hypoxemia and improve V/Q ration (5-20)
46
What is tidal volume
amount of O2 delivered with each ventillation
47
What is fio2
% of o2 delivered with each breath
48
Mechanical Ventilation Complications
ventillator assisted pneumonia
barotrauma
pneumothorax
GI effects
Cardiac effects
49
Causes of pulmonary edema
1. Cardiogenic pulmonary edema
- heart problems (valve problem, CAD, left ventricular dysfunction/failure, fluid overload)
2. Impaired endothelium (lining of capillary)
3. lymphatic obstruction
50
Cardiogenic pulmonary edema
blood backflows into pulmonary vasculature > increased hydrostatic pressure > EDEMA > acute respiratory failure
causes: valve problem, CAD, left ventricular dysfunction/failure, fluid overload
51
impaired endothelium
capillary endothelium - lining of the capillary
hypoalbuminemia: decreases capillary osmotic pressure
OR
injury to capillary caused by:
inhaled toxins, near drowning, inflammation
mechanical ventilation (PEEP, oxygen toxicity)
sepsis
aspiration
smoke inhalation
ARDS
52
lymphatic obstruction
malignancies of the lymph system
lung mass compressing lymph vessels
53
pulmonary edema
fluid in the alveoli displaces air > impaired gas exchange
decreases gas exchange! Oxygen can't cross alveolar/capillary membrane and attach to HGB in capillary
leads to acute respiratory failure!
54
pulmonary edema respiratory symptoms
tachypnea
labored respirations
productive cough *frothy pink sputum*
cough
dyspnea
crackles
paroxysmal nocturnal dyspnea
orthopnea
55
pulmonary edema cardiovascular symptoms
tachycardia
cool, clammy skin
hypotension
hypoexmia
cyanosis
S3
56
pulmonary embolism neurological symptoms
restlessness
feeling of impending doom
anxiety
57
classic symptoms of pulmonary edema - traid
dyspnea, chest pain, hemoptysis (pink/froth sputum)
58
pulmonary edema diagnostic tests
CXR - will see white out
PA catheter (swan ganz) - fluid builds up in the PA. Increased pulmonary artery pressure - will be ELEVATED
Central venous pressure - measures preload - will be ELEVATED
SpO2
ABG
59
Pulmonary edema collaorative care
suctioning (pulmonary toileting)
respiratory support (NC, SFM, VM, non-rebreather)
advanced respiratory support (airvo, cpap, bipap, mechanical vent)
reduce preload
reduce afterload
support perfusion
reverse cause of altered membrane permeabilty
60
How to reduce preload
(decrease fluid in circulation)
diuretics - furosemide oral, IV push, or infusion
nitrates - nitroglycerin vasodilator IV
elevate HOB
61
How to reduce afterload
(improves cardiac output)
calcium channel blockers: amlodipine, verapamil, diltiazem
antihypertensives
nitrates - nitroclycerin, nitroprussside
62
How to support perfusion
increase cardiac output with + ionotropes (increase contraction): dobutamine, digoxin, dopamine
63
how to reverse altered membrane permeability
correct hypoalbuminemia
establish fluid balance
64
Pulmonary hypertension
increased pressure in the pulmonary artery > vascular remodeling
NO cure
can be primary or secondary
65
Primary Pulmonary Hypertension
idiopathic
no known cause
rare
most common in women 20-40
life expectancy 2.8 years from diagnosis without treatment
66
Secondary pulmonary hypertension
2 types: post capillary and precapillary
67
post capillary pulmonary hypertension
distal to (after or beyond) the pulmonary capillaries- LV, LA, pulmonary veins
causes:
LV failure
mitral stenosis
occlusion of pulmonary vein
cirrhosis and portal hypertension
68
Precapillary pulmonary hypertension
problems within the capillaries or alveoli
normally in response to hypoxia - in the lungs pulmonary vessels will CONSTRICT in response to hypoxia
causes related to hypoxia:
COPD
sleep apnea
stiffness of pulmonary vasculature (sarcoidosis)
pulmonary fibrosis
69
Primary Pulmonary Hypertension Manifestations
syncope
dyspnea
fatigue
weakness
chest pain
hemoptysis
activity intolerance
70
Secondary pulmonary hypertension symptoms
looks like underlying problem but more exaggerated
ex: COPD symptoms, CHF symptoms
71
pulmonary HTN diagnostics
echocardiogram - best way
- shows tricuspid regurgitation, RV failure
CXR
- may show enlarged pulmonary artery
Right sided cardiac cath. or insertion of PA catheter
- determine PA pressure
- mean pulmonary arterial pressure will be elevated
72
Pulmonary HTN complications
cor pulmonale ( RV dilation) leading to RV failure
- may present with systemic edema, ascites and weight gain
73
Pulmonary HTN collaborative care
Primary: double lung transplant
Supportive: oxygen spo2 >90
74
pulmonary HTN meds
prostanoids: vasodilators - epoprostenol sodium - continous IV or inhaltion
phosphodiesterase inhibitor/vasodilator: sildenafil
increase cardiac output: digoxin, dobutamine, dopamine
calcium channel blockers (high dose): amplodipine, diltiazem
diuretics: reduces PA pressure
Antcoagulants: warfarin, apixaban, dabigatran
75
epoprostenol sodium side effects
jaw pain, nausea, diarrhea, infection, thromboembolism
76
heparin antidote
protamine sulfate
77
coumadin antidote
vitamin K
78
lifestyle modifcations for pulmonary HTN
low sodium
fluid restriction
low intensity workout
contraception!
avoid temperature extremes
79
pulmonary embolism
thrombus breaks loose from somewhere else and is now an embolus - once it enters pulmonary vessel it will occlude it
usually comes from legs
80
pulmonary embolism origins
blood clot - most common
fat emboli (orthopedic surgery, broken bones)
tumor fragments
amiotic fluid
foreign body
81
Severe PA occlusion
- sudden death "saddle PE"
- lung tissue infarction
82
PE consequences
increased dead space (areas of lungs that are ventilated, but no perfused)
if infarction does not occur, firbinolytic system dissolves clot
PE - Perfusion problem that effects gas exchange
83
DVT risk factors
(virchows triad)
1. venous stasis
- prolonged bed rest, obesity
2. endothelial damage
-vessel wall damage (phlebitis)
3 altered blood coagulation
- inhertied thrombophilia
- cancers that produce coagulation factors
- smoking
- incidence higher in African American
84
PE risk factors
hypercoagulability:
coagulatin disorders
cancer
oral contraceptives
sepsis
following childbirth, sx, trauma
endothelial damage:
phlebitis
surgery
trauma
sepsis
85
pulmonary embolism diagnosis
1. D-Dimer
- indicates high levels of fibrin products in body
2. ABG
- low paO2 and low PaCO2 (hyperventiliation, respiratory alkalosis)
3. CXR
- rule out other condition
4. V/Q scan
- show abnormal perfusion and normal ventilation
5. chest CT with contrast
- difinivie. Can visualize PE
86
pulmonary embolism manifestations
anxiety and apprehension - impending doom
dyspnea & SOB
chest pain
tachycardia/dysrythmia
extremity swelling/pain
tachypnea and shallow respirations
cough
diaphoresis
hemioptosis
87
PE prevention
preophylactic anticoagulants (coumadin, enoxaparin, warfarin)
SCDs
ROM/ambulation
88
PE treatment
support and stablization cardiopulmonary system
- o2
+ionotropes (digoxin, dopamine, dobutamine) if hemodynamically unstable, inadequate output
anticoagulation therapy - haparin, warfarin, apixaban
fibrinolytic therapy if massive PE and patient is hemodynamically unstable
embolectomy
surgery (greenfield) filter
89
ARDS
a group of symptoms: acute lung injury from unregulated systemic inflammatory response to acute injury or inflammation. Part of lung is not getting air
rapid onset of noncardiac pulmonary edema
progressive refratory hypoexemia
extensive lung tissue inflammation
multisystem organ malfunction
90
ARDS mortality rate
smokers more common to acquire
effects men more than women
african americans more often effected
91
direct causes of ards
effect the LUNG
pulmonary infections
aspiration of gastric contents
inhalation injuries (smoke, saltwater, drowning)
92
indirected causes of ards
sepsis (poorer outcomes than respiratory cause)
trauma
GI infections
drug overdose
multiple blood transfusions
severe fluid overload
93
stages of ards
1. initiation of ards (24-48 hours before pulmonary edema) figured out after the fact
2. onset of pulmonary edema
3. alveolar collapse d/t surfactant deficit
4. end-stage ards
94
ards manifestations
intercostal retractions/use of accessory muscles
tacypnea as demand for O2 increases and patient tries to release CO2
adventitious lung sounds (Crackles), edeuma, atelactasis
CXR shows interstitial changes, patchy infiltrates
pulse ox, ABG show refractory hypoxemia
agitation, confusion, lethargy
95
ards diagnostics
ABG to determine o2 levels
CXR or CT to assess fluid in lungs
CBC, blood chemistry, and blood culture to determine cause of ards
sputum culture
blood culture if sepsis suspected
96
ARDS treatment
*intubation - may req. atypical ventilator and high PEEP D/T alveolar collapse and edema
*CPAP/BIPAP
*no definitive drug therapy but maybe:
vasoconstrictors (dopamine, dobutamine)
diuretics
corticosteroids
bronchodilators
NSAIDS
surfactant therapy
* prone position
*ECMO
*insertion of PA catheter
97
why is prone position good for ARDS
decerase dead space
reduces intrathoracic pressure and gravity forces on lung tissue (reduces atelectisis)
enhances ventillation (impoves V/Q matching)
decreases mortalitiy
