-
process w/c supplies cells w/ o2 and removes co2
respiration
-
pulmonary system fails in one or both functions; o2 or CO2 elimination
acute respiratory failure
-
acute respiratory failure is a syndrome or a disease?
syndrome
- can be acute or chronic
- can be hypoxemia or hypercapnic
-
how is acute resp failure defined?
Pao2?
sao2?
paco2?
ph?
- pao2 <60
- sao2 <90%
- paco2 >50
- ph <7.35
-
mechanism of malfunction. name 3
- 1. impaired ventilation
- 2. impaired perfusion
- 3. impaired ventilation & perfusion
-
give examples of what would cause IMPAIRED VENTILATION
-
give examples of what would cause IMPAIRED PERFUSION
- pulmonary edema
- pneumonia
- ARDs
-
give examples of what would cause IMPAIRED PERFUSION AND VENTILATION
-
what is TYPE I RESP FAILURE
hypoxemia
-
what is the issue between ventilation and perfusion in type 1 resp failure?
normal ventilation vs abnormal perfusion
-
type 1 resp failure (hypoxemia)
alveoli?
oxygenation?
commonly involve fluid or collapse of alveoli (CHF, pneumonia)
-
the following conditions can cause which type of respiratory failure:
COPD, obesity, ARDs, pulm edema, pneumothorax, asthma, PE
- type I respiratory failure
- *this is the most common form of respiratory failure
-
normal ventilation vs abnormal perfusion
type I respiratory failure
-
hypercapnic? w/c type of respiratory failure
type II respiratory failure
-
what is the issue of perfusion and ventilation in type II resp failure?
normal perfusion vs. abnormal ventilation
-
in type II respiratory failure, there is an issue with ventilation. t or f?
true
insufficient ventilation - pt isn't breathing, not blowing off co2 (hypercapnic)
-
this following conditions may cause w/c type of respiratory failure:
COPD, poisoning, myasthenia gravis, pulmonary edema, obesity, drug overdose, ARDS
type II respiratory failure
-
normal perfusion vs. abnormal ventilation
type II respiratory failure
-
s/s on the CNS during assessment for acute respiratory failure
- RESTLESS
- confusion
- irritability
- IMPENDING DOOM
- somnulence
- *co2 accumulates
-
s/s on the respiratory system in acute resp failure
- dyspnea - sob, difficulty
- increased depth = hypoxemia
- decreased depth = hypercapnia
-
s/s on cardiovascular system in acute resp failure
- tachycardia - early
- HTN - early
- bradycardia - late
- hypotension - late
- arrhythmias
-
dx tests for acute respiratory failure
- abgs - ph < 7.35; po2 <60; pco2 >50
- chest xray
- sputum culture, cbc, electrolytes
- ecg
-
nursing care for acute respiratory failure
- PREVENTION:
- treat cause
- airway - clearance
- breathing patterns
- IMPROVE OXYGENATION:
- o2
- airway adjuncts - endotracheal tube and ventilation
MAINTAIN OPTIMAL CARDIAC OUTPUT
-
other nursing interventions for acute resp failure
- SCD
- IS 10x/hr
- deep breathe, cough
- ambulation
- control pain = ^ breathing
-
syndrome of lung inflammation and injury, potentially fatal non-cardiac pulmonary edema
acute respiratory distress syndrome (ARDS)
-
characteristics of ARDS
hypoxemia?
rr?
alveoli?
xray?
PCWP?
- acute and refractory hypoxemia (despite 100% FIO2)
- tachypnea
- decreased lung compliance
- alveolar collapse
- bilateral infiltrates on xray "white out"
- PCWP <18 mmhg
-
pathophysiology of ARDS
activation of systemic inflammatory response syndrome (SIRS) in response to direct or indirect lung injury
-
phases of ARDS
- 1. acute exudative phase
- 2. proliferative phase
- 3. fibrotic phase
-
ARDS: this phase there is damage to alveolar epithelial cells. fluid accumulates in alveoli
acute exudative phase
-
ARDS: this phase the damage spreads from base to upper lobes
proliferative phase
-
ARDS: this phase damage to the alveoli; scarring; alveoli can no longer open and close
fibrotic phase
-
name some direct causes that can lead to alveolar injury and inflammation
- aspiration
- inhalation injury
- contusion
- embolism
- radiation
- reperfusion injury
- o2 toxicity
-
name some indirect causes of ARDS: activation of SIRS outside the lung; tissue destructive cytokines travel to the lungs
- shock
- sepsis
- trauma
- pancreatitis
- drug OD
- massive blood transfusion
- disseminated intravascular coagulopathy
-
dx of ARDS:
ABNORMAL CHEST XRAY
- ABNORMAL ABGS
- early resp alkalosis
- later resp acidosis
- eventually metabolic acidosis
- REFRACTORY HYPOXEMIA
- despite supplemental o2
- ABNORMAL PUMONARY FUNCTION TEST
- decrease compliance
- decrease FRC (functional residual capacity
*might hear crackles or NOTHING
-
early ABGs in ARDS?
respiratory alkalosis
-
later ABGs in ARDS?
- respiratory acidosis
- eventually leads to METABOLIC ACIDOSIS
-
nursing care for ARDS
1. collaborative management
- 2. support and improve oxygenation
- -mechanical ventilation
- -medications
- -positioning
3. nutritional support BIG NEED
- 4. prevention of complications
- -multi-organ system dysfunction/failure
- -ventilatore acquired pneumonia
-
a collection of particulate matter that enters the venous system and lodges in the pulmonary vessels
pulmonary embolism
- can be:
- fat
- amniotic fluid embolism
- blood clot
-
pathophysiology of PE
- thrombus formation
- portion of clot dislodges
-
name some causes of clot formation and dislodge
- vena caba
- R side of heart
- occlusion of pulm vessel
- ventilation (V/Q) mismatch
- pulmonary vessel constriction
- pulmonary hypertension
- decreased surfactant
- atelectasis
- pulmonary infarction
-
what is VIRCHOW'S triad
- 1. venous stasis
- 2. endothelial damage
- 3. hypercoagulability
-
some factors that may cause VENOUS STASIS
- immobility
- obesity
- advanced age
- varicose veins
- blockage/compression of femoral or iliac vein
-
some factors that may cause ENDOTHELIAL DAMAGE
- CENTRAL VENOUS CATHETERS
- HX OF dvt
- trauma
- surgery
-
what may cause HYPERCOAGULABILITY
- pregnancy
- estrogen tx
- CVA
- fam hx
-
turner's syndrome?
hint: dvt
femoral artery easily compresses = clot formation
-
s/s of PE
- restless
- apprehension
- impending doom
- cough
- hemptysis
- tachypnea
- fever
- diaphoresis
- pleural friction rub
- petechiae
- s3 or s4
- decrease sao2
- dyspnea, abrupt onsent
- pleuritic chest pain
- tachycardia
-
DX of PE
abnormal ABGs (same as ARDS)
- early resp alkalosis
- later resp acidosis
- eventually metabolic acidosis
- abnormal chest xray (may see large emboli)
- infiltrates
abnormal angiogram
increased wbc
positive d-dimer
-
goal of nursing care for PE
improve ventialtion and perfusion, minize risk of additional clot formation, prevent complications
-
nurse interventions for PE:
assessments?
clots?
surgery?
respiratory assessment - crackles, admin o2
cardiac assessment - s3; s4
anticoagulation meds - iv heparin, warfarin, thrombolytic
surgical management - vena cava filter
*antidote - predatine sulfate
-
influenza:
who's at risk?
caused by what?
- older adults
- debilitated
- immunocompromised
caused by ABC
-
highly contagious acute viral respiratory infection
flu
-
the following sx of manifestations of what:
severe HA, muscle ache, fever, chills, fatigue, wekaness, anorexia
flu
-
how to prevent influenza
vaccines
antivirals may be effective
-
when is someone contagious with the flu?
from 24 hrs before sx and up to 5 day s after they begin
-
nursing care for the flu
- prevention
- education
- vaccination
- handwashing
-
excess fluid in the lungs resulting from an inflammatory process
pneumonia
-
what may be the cause of inflammation in pneumonia
- infectious organism
- inhalation of irritants
-
where can one get pneumonia
- community acquired pneumonia (CAP)
- nosocomia or hospital acquired (HAP)
-
what manifesations does pneumonia have
- atelectasis
- hypoxemia
- dyspnea
- cough
- sputum
- fever
- pleuritic chest pain
-
which is more common, community or hospital acquired pneumonia?
CAP, occurs late fall and winter as complications of influenza
*HAP has 10-50% mortality rate
-
dx for pneumonia:
- gram stain, culture, sensitivity testing of sputum
- cbc
- abgs
- serum bun level
- electrolytes
- creatinine
- imaging assessment (CXR)
- pulse ox
-
nurse interventions/treatment of pneumonia
- o2
- IS
- meds - antiinfectives, bronchodilators
- avoid dehydration
- teaching, prevetnion (pt and staff)
- vaccination
- HANDWASHING
-
a syndrome of acute resp failure (non cardiogenic pulmonary edema) that can be triggered by a wide variety of conditions:
- direct pulmonary trauma
- indirect pulmonary trauma
-
patho of ARDS: 2 main insults to lungs
- 1. alveolar-capillary membrane damage
- 2. decreased surfactant production -> decreases lung compliance "stiff lungs"
-
early clinical manifestations of ARDS
- tachypnea
- tachycardia
- dyspnea
- confusion
- agitation
- fine crackles
-
later clinical manifestations of ARDS
- diffuse crackles
- rhonchi (gurgles)
- cyanosis
-
occlusion of portion of the pulmonary arterial bed by a thrombus or other foreign
pulmonary emboli
-
the air that reaches the lungs
ventilation
-
the blood that reaqches the lungs
perfusion "Q"
-
since it is difficults to keep SAo2 above 90% in ards. we need extra measures. what is this?
PEEP (positive end expiratory pressure)
-
the purpose of PEEP (positive end expiratory pressure) ?
helps keep alveoli expanded inspite of inflammation and fluid levels
-
what can happen if PEEP is too low?
alveoli will collapse w/ every exhalation
-
what can happen if PEEP IS TOO HIGH
- trauma to alveoli
- decreased CO (actual pressure on heart form constantly air filled bronchi and airways)
- decrease surfactant production
- impede capillary blood flow at alveolus
- worse V/Q matching if not balanced well
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