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115 Cards in this Set

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inc/dec surface tension?
decreased surface tension=increased lung compliance making it easier for lungs to inflate
how does surfactant aid in preventing pulm edema?
keeps alveoli dry
Dx notorious for decreasing surfactant prod
Dec surfactant=inc surfacae tension and dec lung compliance making it harder for lungs to inflate
Dx's that can decrease lung compliance
COPD (fibrosis), ARDS (via dec surfactant)
What role does slight negative intrapleural pressure serve
Helps keep alveoli open
What might increase airway resistance
Pulmonary secretions, bronchospasms.
Small changes in diameter can lead to enormous changes in flow (ventilation) and thus inc WOB
fx of hypervent on PaCO2
decreases PaCO2 (alkalotic)
fx of hypovent on PaCO2
increases PaCO2 (acidosis)
term for air w/in conducting airways that ultimately does not reach alveoli
anatomical dead space (often assoc w/ COPD)
Intervention for decreasing anatomical dead space
dependant upon body position****
Terminolgy when perfusion is decreased/absent but ventilation is normal
Physiological/alveolar dead space
AKA for physiological dead space
Alveolar dead space i.e. decreased/absent perfusion
physiological dead space AKA alveolar dead space refers to
1) decreased/absent perfusion
2) decreased ventilation
1) decreased/absent perfusion
Som factors that may thicken capillary membrane and fx diffusion of gasses
secretions, intersitial lung Dx, pulm edema
Best overall body position for VQ matching
Semi folwers
physiologic shunt. Problem with
Physiologic shunt.
1) high VQ (vent>perfusion)
2) low VQ (perfusion>vent)
Low VQ
Problem with ventilation/alveoli so,
Blood is passing by alveoli wihtout gas exchange
Term for VQ imbalance when adeq bf is passing by alveoli but gas exchange is not occuring
Physiologic Shunt
Problem with Alveoli
Low VQ (perrfusion>vent)
Cndx's causing physiologic shunt
Think about condz's reducing ventilation
Mucus plug
Alveolar/physiologic dead space. Problem with
1) bf
2) alveoli
Blood flow
Alveolar/physiologic dead space.
1) High VQ (vent>perfusion)
2) Low VQ (perfusion>vent)
High VQ
problem with bf so,
High VQ (ventil>perfusion)
term for VQ imbalance when blood flow to alveoli is reduced and gas exchange can not occur
Alveolar/physiologic dead space
problem with b.f.
High VQ (ventil>perfusion)
Condx's causing alveolar dead space
PE r/t blockage
Cardiogenic shock (dec CO and thus poor lung perfusion)
Pulm HTN
Mechanical vent (increases intrathoracic pressure)
Silent unit. Problem with
1) bf
2) alveoli
Dec in both vent and perfusion
Cndx's causing silent unit
represents amt of O2 dissolved in plasma
Normal PaO2
Normal SaO2
93 or greater
represents the amt of hemoglobin molecules bound with O2
Most O2 supplied to tissues as PaCO2 or SaO2
PaO2<?? = large changes in SaO2
More negative fx for pt
1) High affinity of O2 for Hb
2) Low affinity of O2 for Hb
High affinity
At tissue level tight bond does not readily release O2
stims inspir/expir of diaphragm and itnercostals
controls apneustic center and pneumotaxic center
chemoreceptros in periphery stim increased respirs when PaO2<??
Causes decreased SvO2
May indic
1)decreased o2 supply
-dec H&H
-Dec CO
-dec arterial sat
2) increased O2 usage
Resp acidosis caused by
1) CNS depression r/t head inj, sedatives/analgesia/narcotics
2)Pulm d/o i.e. PE, COPD, pneumonia, pulmonary edema
3) Pain
Mgmt/Tx of resp acisdosis
MV usually all thats required
Other measures
-Pain mgmt
-Pulm toilet
What is done in pulmonary toilet
-Increase HOB
-Secretion removal -Cough/deep breath
-Incentive spirometry
Causes resp alkalosis
Panic attacks
Causes tetany (hypoCa)
1) alkalosis
2) acidosis
Mgmt/Tx resp alkalosis
Ativan if anxiety d/o
Paper bag/rebreather
Pain mgmt
Causes of increased acids in metab acidosis
Renal failure-
Anerobic metab>inc lactic acid secondary to lack of O2 to tissues
Salicylate toxicity
Causes of loss of base in metab acidosis
Kussmaul's respirs assoc with what acid/base d/o
Metab acidosis/DM/ketoacidosis
Compens mech to try and blow off acid/CO2
Mgmt/Tx metab acidosis
Treat underlying d/o (ketoacidosis, renal failure, hypoxia/anerobic metab)


IV sodium bicarb
IV sodium bicarb indic in what acid/base d/o
Metab acidosis
Diamox indic in what acid/base d/o
Metab alkalosis
Which acid/base d/o most requires cardiac monitoring
Metab acidosis-lots of arrhythmias
What may cause loss of acids in metab alkalosis
Excessive vomiting/NG suction
What might lead to gain of base in metab alkalosis
Excess bicarb in codes
Mgmt/Tx metab alkalosis
Tx underlying cause
-excess: bicarb, suction, diuretics
O2 flow with nasal cannula
O2 flow with simple face mask
O2 flow with non-rebreather
12-15 (although still technically not 100%)
example of high flow O2 delivery system
-Most reliable and accurate method for precise concentrations of O2
-Constant O2 is inhaled despite pt’s RR and depth of respires
O2 toxicity a concern when FiO2 is > ?? for ?? long
Goal is to titrate to lowest setting while maintaining PaO2>60 or SpO2>92
O2 toxicity carries risk of
Alveolar capillary leakage leading to pulmonary edema
Measures to prevent vomit/aspiration druing ETT placement
Suction and sedation
Why is it impt to monitor for SpO2, HR and BP during ETT placement
Arrhythmia (hypoxemia)
Cardiac arrest
Measures to ck placement of ETT
Auscultate (evaluate for R main stem intubation-would only hear l.s. on one side)
CXR (203 cm above carine)
indications for suctioning
-Dec SaO2
-Vent alarms
-Visual observance of secretions
Acute resp failure


Resp acidosis with hypoxemia
Causes of hypoxemic resp failure
V/Q mismatch-Physiologic shunt (not a prob with blood flow)
Partially collapsed alveoli, alveoli filled with fluid
Pnemonia, atelectasis, mucus plug
This diagnostic study assists in confirming type (I, II, III) of acute resp failure
1st line Tx to correct resp acidosis in acute resp failure
Increase alveolar ventilation and pulm toilet
MV-blow off O2
Tx underlying Dx process (pneumothorax, head injury)
Nute support in acute resp failure pt
Little carbs
Why are carbs not increased in enteral feeds with acute resp failure/ARDS
Carbs increase CO2 production
3 criteria for Dx of ARDS
-Hypoxia refractory to FiO2 admin
-Non-cardiogenic pulm edema-PAWP <18 (>18 would indic HF)
-CXR consistent with bilat infiltrate AKA white out
Examples of direct pulmonary injury in ARDS
Aspiration of gastric contents
Pulmonary infection
Example of indirect pulmonary injury in ARDS
-Shock/Sepsis-Big risk, majority end up in ARDS
Type of V/Q mismatch in ARDS
Silent unit
1)Intrapulm shunt
-Alveolar/capillary membrane damage>alveolar edema
-Dysfxnal surfactant>alveoli not open/dry
-mediator induced bronchoconstriction
2) Alveolar dead space (decreased lung perfusion)
-Pulm HTN
Stage 1 (1st 12 hours)manifestations of ARDS
Hardly any
1) Increased SOB and RR mimics many other Dx processes
2) CXR normal showing no cellular damage
Stage at which CXR begins to show patchy infiltrates in ARDS
2-withing 24 hours of onset
Also refractory to O2 requiring MV
Stage at which ARDS becomes resistant to O2 admin and requires mechanical vent
2-within 24 hours
Also CXR begins to show patchy infiltrates
ARDS stage at which you begin to see hemodynamic instability
3-2-10 days
FiO2 req continues to increase as well as need for PEEP
White shows on CXR
Stage at which white shows on CXR in ARDS
3-2-10 days
Hemodynamic instability seen
FiO2 req continues to increase as well as need for PEEP
Early ABG's in ARDS
Resp alkalosis
Resp acidosis dvp's as ventilation worsens and continues to get worse despite interventions
PaO2 in ARDS
<6o and gets worse despite increasing FiO2
In ARDS transfuse when Hb<??
Improves O2 delivery
Controversial method of improving CO in ARDS
Fluid administration b/c of SIRS mediated vasodil


Potential for 3rd spacing d/t SIRS endothelial changes
Get Swann
Pharmacological means of increasing CO in ARDS
Inotropes-dopa, dobuta
Pressors-dopa (high dose, norepi, levophed
MV settings in ARDS
-Probably FiO2 of 100% (would like to titrate down if possible but usually not possible)
-Small tidal volume to account for still lungs
-PEEP 10-15
Term for prone+kinetic
rotation<40 degrees
Continuous lateral rotation
rotation>40 degrees
Benefits of prone positioning in ARDS
-Pulls perfusion to anterior portion of lungs thereby increasing oxygenation
-CXR resolution
Rx for ARDS
None specific
-Steroids-decrease inflammation in lung and intravasc tissue
-Abx for VAD prophylaxis
Etiology of protein wasting in ARDS
1) SIRS allows for protein wasting via capillary leakage
2) Mediators release proteolytic enzymes which stim catabloism
-Promot nute therapy essential
# of kcal/kg/day in ARDS
2 pt populations at great risk for PE
Post surg (specifically hip/knee)
ICU pt's in general d/t immobility
Virchows triad
1) Venous stasis>clots
2) Hypercoagulabilty-immobiliz secondary to surgery
3) Endothelial changes e.g. incisions
Majority of PE/DVT arise from?
Type of V/Q mismatch in PE
Alveolar/physiological dead space i.e. problem with perfusion d/t occlusion of PA artery
In PE hemodynamic changes occur when blockage>??
In PE Hemodynamic changed b/c severe when blockage>??
What hemodynamic parameters change in PE
Normal PAP
20-30/8-15 (20-30)
Normal CVP
Normal PAWP
S&S of DVT
Does not affect pulses
S&S absent in 25%
Most common manifestations of PE
SOB and inc RR (very non-specific)
Test of choice in PE with stable pt
VQ scan
Test of choice in unstable pt
Pulm angiography
Gold standard for Dx in PE
Pulm angiography
Nursing interventions/monitoring for Pulmonary angiography
BUN/Creat r/t die
Emergent mgmt of PE
Establish airway/IV
Maintain CO
Prepare diagnostic test
When are thrombolytics indic in PE
massive PE/hemodynamically unstable
C/I to thrombolytics in PE
cranial bleed
recent surgery (which may be highly likely)
Nursing interventions/monitoring for thrombolytics in PE
Get foley, NG/DT, IV's in before initiation
Watch for bleed
Monitor vitals
PTT goal with heparin in PE
1.5-2.5 X normal
45-70 sec
Indication for IVC filter
Chronic/recurrent PE/DVT
S&S of IVC filter clotting
Increasing LE edema
In ARDS, what causes decreased lung compliance
Surfactanct production inhibited>surface tension increases>lungs become harder to inflate

Ventilatory capacity is decreased
PAWP must be < ?? for ARDS to be Dx'd
18 i.e. non cardiogenic pulm edema