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CRITICAL CARE OVERVIEW OFRESPIRATORY SYSTEM
RESPIRATORY FAILURE ACUTE EXCASERBATION OF ASTHMA
PULMONARY OEDEMA
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INFECTION
RESPIRATORY
CARDIAL GI TRACT
METABOLIC
HEMATOLOGIC INTOXICATION
NEUROLOGIC
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OBSTRUCTION COPD, ATSHMA, CORPUS ALIEN
RESTRICTIONS COLLAPS, ATELECTASE
PNEUMOTHORAC
PLEURAL EFFUSION BILATERAL
ARDS
RESPIRATORY FAILURE TB, CARSINOMA
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NON INVASIV
MEDICAL
INVASIV Surgical , non surgical
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ENDOTRACHEAL TUBE
MECHANICAL VENTILATION
EMERGENCY BRONCHOSCOPY EMERGENCY THORACOSCOPY
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Invasive
Criteria
Complication
Prognosis
Recovery
High cost
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1. Look
1. Clinical finding
2. Anamnesis2. Asseswhats the problem, etiology
3. Priority problem
4. ABC5. AIR WAY, BREATHING
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1. Define and classify acute respiratory failure.
2. Review the causes of acute respiratory
failure.
3. Describe the pathophysiology of acute
respiratory failure.
4. Highlight the clinical presentation of acuterespiratory failure.
5. Outline management strategies in acute
respiratory failure.
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acute respiratory failure occurs when:
pulmonary system is no longer able to meet themetabolic demands of the body
hypoxaemic respiratory failure:
PaO2 50 mm Hg when breathing room air
hypercapnic respiratory failure:
PaCO2 50 mm Hg.
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Two basic types of respiratory failure:hypoxemic and hypercapnic
Hypoxemic respiratory failure is defined bya room air PaO2 of
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Depends on PAO2 FIO2
PACO2
Alveolar pressure
Ventilation
Diffusing capacity
Perfusion
Ventilation-perfusion matching
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Largely dependent on alveolarventilation
Anatomical deadspace constant butphysiological deadspace depends onventilation-perfusion matching
)V-(VxRRnventilatioAlveolar DT
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Respiratory rate
Tidal volume
Ventilation-perfusion matching
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FIO2
Ventilationwithout
perfusion
(deadspaceventilation)
Diffusionabnormality
Perfusionwithout
ventilation(shunting)
Hypoventilation
Normal
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FIO2
Ventilationwithout
perfusion
(deadspaceventilation)
Diffusionabnormality
Perfusionwithout
ventilation(shunting)
Hypoventilation
Normal
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75% 75%
100% 75%
87.5%
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Intra-cardiac
Any cause of right to left shunt
eg Fallots, Eisenmenger
Intra-pulmonary
Pneumonia
Pulmonary oedema
Atelectasis Collapse
Pulmonary haemorrhage or contusion
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Intra-pulmonary Small airways occluded ( e.g asthma, chronic
bronchitis)
Alveoli are filled with fluid ( e.g pulm edema,pneumonia)
Alveolar collapse ( e.g atelectasis)
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FIO2
Ventilationwithout
perfusion
(deadspaceventilation)
Diffusionabnormality
Perfusionwithout
ventilation(shunting)
Hypoventilation
Normal
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Dead space ventilation
Alveoli that are normally ventilated but poorly perfused
Anatomic dead space
Gas in the large conducting airways that does not come incontact with the capillaries e.g pharynx
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DSV increase:
Alveolar-capillary interface destroyed
e.g emphysema Blood flow is reduced e.g CHF, PE
Overdistended alveoli e.g positive-
pressure ventilation
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FIO2
Ventilationwithout
perfusion
(deadspaceventilation)
Diffusionabnormality
Perfusionwithout
ventilation(shunting)
Hypoventilation
Normal
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Less common
Abnormality of the alveolar membrane or a
reduction in the number of capillaries resulting ina reduction in alveolar surface area
Causes include:
Acute Respiratory Distress Syndrome
Fibrotic lung disease
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FIO2
Ventilationwithout
perfusion
(deadspaceventilation)
Diffusionabnormality
Perfusionwithout
ventilation(shunting)
Hypoventilation
Normal
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Brainstem
Spinal cord
Nerve rootAirway
Nerve
Neuromuscular
junction
Respiratorymuscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
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Respiratory failure acute / chronic
depending on the duration and the
nature of the compensation.ARF may occur in a person without
previous lung disease or may besuperimposed on chronic respiratory
failure
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ARF develops in a variety of clinicalsettings
primary pulmonary insults other systemic nonpulmonary disorders
Causes of ARF in adults are often
multifactorial. Mixed
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Hypoxemic respiratory failure is seen inpatients with acute lung injury (ali) or
acute pulmonary edema (cardial /noncardial).
These disorders primarily interfere with thepulmonary system's ability to adequately
oxygenate the blood as it circulatesthrough the alveolar capillaries.
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Hypercapnic respiratory failure is seen inpatients with
severe airflow obstruction, central respiratory failure, or
neuromuscular respiratory failure.
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result of a mismatch of alveolarventilation and pulmonary perfusion
cause progressive obstruction oratelectasis result in less oxygen beingavailable in distal airways for uptake
blood flow to such abnormal lung unitsdeclines
e.g., pneumonia, aspiration, edema, etc
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Other less common causes of hypoxemiainclude:
Decreased diffusion of oxygen acrossthe alveolocapillary membrane complexdue to interstitial edema, inflammation,etc.
Alveolar hypoventilation
High altitude.
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When gas flow to and from airwaysremains adequate but blood flow is
absolutely or relatively diminished, C02does not have the opportunity to diffusefrom the pulmonary artery blood andC02-rich blood is returned to the left
atrium.
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Increased deadspace ventilation mayoccur in :
hypovolemia, pulmonary embolus,
poor cardiac output, or
when the regional airway pressure isrelatively higher than the regionalperfusion pressure produced by theregional pulmonary blood flow
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Several related disease processes oftencombine and act in concert or
synergistically to compound respiratoryfailure.
For example, the patient with chronicpulmonary disease (COPD) and often
has associated heart failure (CHF) whichincreases worsens hypoxemia
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ARDS is another type of acute respiratoryfailure
Increased alveolar capillary permeabilityin ARDS have centered upon
the neutrophil,
the macrophage,
the pulmonary vascular endothelium and
The cytokine imbalance
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Neutrophil sequestration and migrationwithin the lung remain histologic
hallmarks of ARDS Chemotactic stimuli released within the
lung and the activation of neutrophils bycirculating mediators :
TNFa ,
IL-1, and
IL-8
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There are 5 extremelyaccurate objectiveindicators ofrespiratory distress:
retractions
tachycardia > 130
pallor/cyanosis
altered mental
status absent breath
sounds
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Wheezes
Rales/crackles
Rhonchi/lowwheezes
Pleural friction rub
Stridor
Absent!!!
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Altered mental status ranging from agitation to
somnolence
Evidence of increased work of breathing:
nasal pharing
use of accessory respiratory muscles
intercostal/suprasternal/supraclavicular retraction
Tachypnea
Hyperpnea
paradoxical or dysynchronous breathing pattern
Cyanosis of mucosal membranes (tongue,
mouth) or nail beds
Diaphoresis, tachycardia, hypertension and other signs
of "stress" catecholamine release
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The assessment skills we have discussed sofar are the keys to excellent pulmonaryassessment. However, there are several
diagnostic tests that may also play a rolein these cases:
Pulse Oximeter
Peak flow ABGs
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Arterial blood yields information
regarding:
acid/base status ventilation
oxygenation
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But first, why evaluate ABGs?
To determine acid/base status (pH)
To evaluate adequacy of ventilation(PaCO2)
To evaluate adequacy of oxygenation(PaO2)
To understand whether the abnormality islong-standing or extremely acute (HCO3)
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Normal values (room air, sea level)
pH 7.35 - 7.45
paCO2 35 - 45 torr
paO2 75 - 100 torr
HCO3
-24 - 35 mEq/L
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Step 1: Acid/Base Status Look at the pH. Is it normal or abnormal?
If abnormal, is it acid orbase?
< 7.35: acid
> 7.45: base
Write it down!
Note: an abnormal pH is always an acuteevent. No one has a chronically abnormalpH!
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Step 2: Respiratory Component
Look at the PaCO2. Is it normal orabnormal?
If abnormal, is it tending toward acid orbase?
< 35: base
> 45: acid Write it down!
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Step 2: Respiratory Component
Note: the PaCO2 also tells us aboutventilation. If it is below normal, in mostcases minute ventilation should bedecreased (slow rate, reduce tidal volume).If it is too high, increase minute ventilation.
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Step 3: Metabolic Component
Look at the HCO3. Is it normal or abnormal?
If abnormal, is it tending toward acid orbase?
< 22: acid
> 26: base
Write it down!
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Step 3: Metabolic Component
Note: HCO3 also tells us about chronic vs.acute. Acute episodes dont have time toactivate the kidneys, so the HCO3 is normal.Long-standing conditions alter kidneyfunction, and will change HCO3.
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Step 4: Oxygenation Look at the PaO2. Is it normal or abnormal?
If the PaO2 is below normal (
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Step 5: Put it all together
Look at the pH, PaCO2, and HCO3.
Identify any changes which are consistentwith the pH abnormality. They are the cause.
Youve now identified the problem as either:
Respiratory (PaCO2 change is consistent with pH)
Metabolic (HCO3 change is consistent with pH)
Mixed (Both are consistent with pH)
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Oxygen Supplementation
Nasal Cannula
Air-Entrainment Face Masks ("Venturi Masks") Aerosol Face Mask
Reservoir Face Masks
Noninvasive Positive-Pressure Ventilation
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Do not use NPPV for rapidly deterioratingpatients at risk for sudden respiratoryarrest.
Do not use NPPV unless the physician orrespiratory care practitioner is familiarwith its technical operation.
Consider NPPV primarily in alert,oriented, hemodynamically stable, andcooperative patients.
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1.Beta2-Agonists
2.Anticholinergic Agents
3.Corticosteroids 4.Theophylline preparations
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Gagal napas
- PaCo2 > 60 torr
- Ratio Pa O2/FiO2 : < 200 : ARDS
< 300 : ALI
- RR > 30 menit
Syok
+ ventilator mekanik
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ACUTE EXACERBATION OF
ASTHMA
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Nighttime awakenings
Need for short-acting 2-agonists (SABAs) for quick reliefof symptoms
Work/school days missed
Ability to engage in normal dailyactivities or desired activities
Quality-of-life assessments
Symptoms
Spirometry
Peak flow
Lung Function
Impairment = Frequency and Intensity ofSymptoms and Functional Limitations
Adapted from 2007 NHLBI Expert Panel Guidelines (EPR-3).
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Likelihood of asthma exacerbations, progressivedecline in lung function, or risk of adverse effectsfrom medications
Assessment Frequency and severity of exacerbations
Oral corticosteroid use
Urgent-care visits
Lung function
Noninvasive biomarkers may play an increased role infuture
Adapted from 2007 NHLBI Expert Panel Guidelines (EPR-3).
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ImpairmentClassification of Asthma Control
Well Controlled Not Well Controlled Very Poorly Controlled
Symptoms 2 days/week > 2 days/weekThroughout
the day
Nighttime
awakenings
2x/month 13/week 4/week
Interference with
normal activityNone Some limitation Extremely limited
Short-acting
2-agonist
use for
symptom control
2 days/week > 2 days/weekSeveral times
per day
FEV1 or
peak flow
> 80% predicted/
personal best
6080% predicted/
personal best
< 60% predicted/
personal best
Adapted from 2007 NHLBI Expert Panel Guidelines (EPR-3).
Patients 12 years of age
Bagan Terapi Asma Saat Ini
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Pengontrol(Controller)
Pelega (Reliever)
Terapi harian multi obatSteroid inhalasi (ICS)
Long Acting 2 -agonist (LABA)Oral steroid
Menghindari faktor pencetus
Terapi harian
Steroid inhalasi (ICS)
Long Acting 2 -agonist (LABA)
Terapi harianSteroid inhalasi (ICS) Inhalasi 2-agonis prn
Tingkat 2: PERSISTEN RINGAN
Tidak perlu Inhalasi 2-agonis prn
Menghindari faktor pencetus
Menghindari faktor pencetus
Menghindari faktor pencetus
Tingkat 1: INTERMITEN
Inhalasi 2-agonis prn
Tingkat 4: PERSISTEN BERAT
Inhalasi 2-agonis prn
Tingkat 3: PERSISTEN SEDANG
Bagan Terapi Asma Saat Ini
Naikkan dosis jika
tidak terkontrol
Turunkan dosisketika terkontrol
Penyesuaian dosis
setelah 3 bulan terkontrol
harus tetap
dimonitor/evaluasi
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Early treatment is best. Importantelements include: A written action plan
Guides patient self-management ofexacerbationsat home
Especially important for patients withmoderate-to-severe persistent asthma and
any patient with ahistory of severe exacerbations
Recognition of early signs of worseningasthma
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Appropriate intensification of therapy
Prompt communication between patient
and clinician about:
Serious deterioration in symptoms or peakflow, or
Decreased responsiveness to inhaledbeta2-agonists, or
Decreased duration of beta2-agonist effect
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Inhaled beta2-agonist to provideprompt relief of airflow obstruction
Systemic corticosteroids to suppressand reverse airway inflammation
For moderate-to-severe exacerbations, or
For patients who fail to respond promptlyand completely to an inhaled beta2-agonist
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Past history of sudden severeexacerbations
Prior intubation or admission to ICUfor asthma
Two or more hospitalizations forasthma
in the past year Three or more ED visits for asthma
in the past year
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Hospitalization or an ED visit for asthmain the past month
Use of >2 canisters per month ofinhaled short-acting beta2-agonist
Current use of systemic corticosteroids
or recent withdrawal from systemiccorticosteroids
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Difficulty perceiving airflow obstructionor its severity
Comorbidity, as from cardiovasculardiseases or chronic obstructivepulmonary disease
Serious psychiatric disease orpsychosocial problems
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Low socioeconomic status andurban residence
Illicit drug use Sensitivity toAlternaria
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Develop a written action plan with
each patient, especially thosewith:
Moderate-to-severe persistent asthma or
History of severe exacerbations
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The plan should include:
Signs, symptoms, and peak flow levels that indicatedeteriorating asthma
How to adjust medications in response todeteriorating asthma
When to seek medical help
Emergency phone numbers
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Use inhaled short-acting beta2-agonist:
Up to three treatments of 2 to 4 puffs byinhaler at 20-minute intervals
OR
Single nebulizer treatment
Assess symptoms and/or peak flow
after 1 hour
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Peak flow >80% predicted or personal
best and/or No wheezing, shortness of breath,
cough, or chest tightness and
Response to beta2-agonist sustainedfor4 hours
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May continue 2 to 4 puffs beta2-agonist
every 3 to 4 hours for 24 to 48 hours PRN
For patients on inhaled corticosteroids,
double dose for 7 to 10 days
Contact clinician within 48 hours forinstructions
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Peak flow 50% to 80% predicted or
personal best or
Persistent wheezing, shortness ofbreath, cough, or chest tightness
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Take 2 to 4 puffs beta2-agonist every
2 to 4 hours for 24 to 48 hours PRN Add oral corticosteroid for 3 to 10
days, at least until symptoms andpeak flow are stable
Contact clinician urgently (same day)for instructions
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Peak flow
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IMMEDIATELY
Take up to three treatments of 4 to 6puffs beta2-agonist every 20 minutes PRN
Start oral corticosteroid
Contact clinician Go to emergency department or
call ambulance or 9-1-1
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Correction of significant hypoxemia
Rapid reversal of airflow obstruction
Reduction of likelihood of recurrence
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FEV1 or PEF 50% to 80% predicted
or personal best
Physical exam: moderatesymptoms
Inhaled short-acting beta2-agonist
every 60 minutes
Systemic corticosteroid
Continue treatment 1 to 3 hours,
provided there is improvement
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FEV1 or PEF
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FEV1 or PEF >70%
Response sustained 60 minutes
after last treatment No distress
Physical exam: normal
Discharge Home
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FEV1 or PEF >50% but
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FEV1 or PEF 42 mm Hg
Physical exam: symptoms severe,drowsiness, confusion
Admit to hospital intensive care
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Inhaled beta2-agonist hourly or
continuously + inhaled anticholinergic
IV corticosteroid
Oxygen
Possible intubation and mechanicalventilation
Admit to hospital ward
Step Up dan Step Down Therapy of
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Step Up dan Step Down Therapy ofAsthma
Reliever: Rapid-acting inhaled 2-agonist prn
Controller:
Daily inhaled
corticosteroid
Controller:
Daily inhaledcorticosteroid
Daily long-acting inhaled2-agonist
Controller:
Daily inhaledcorticosteroid
Daily long acting inhaled2-agonist
plus (if needed)
Whenasthma iscontrolled,reducetherapy
Monitor
STEP Down
Outcome: Asthma Control Outcome: BestPossible Results
Controller:
None-Theophylline-SR
-Leukotriene
-Long-acting inhaled
2
- agonist
-Oral corticosteroid
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A 62-year-old man presents with a three-day history of progressive dyspnea,nonproductive cough, and low-grade
fever Congestive heart failure history
His blood pressure is 95/55 mm Hg, hisheart rate 110 beats per minute, histemperature 37.9 degreesC, and hisoxygen saturation while breathingambient air86 percent
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Chest auscultation reveals rales andrhonchi bilaterally
A chest radiograph shows bilateral
pulmonary infiltrates consistent withpulmonary edema and borderlineenlargement of the cardiac silhouette
How should this patient be evaluated toestablish the cause of the acutepulmonary edema and to determineappropriate therapy
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Pulmonary edema is a condition
characterized by fluid accumulation in the
lungs caused by back pressure in the lung
veins. This results from malfunctioning of theheart.
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Pulmonary edema is a complication of a
myocardial infarction (heart attack), mitral or
aortic valve disease, cardiomyopathy, or
other disorders characterized by cardiacdysfunction.
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Fluid backs up into the veins of the lungs.
Increased pressure in these veins forces
fluid out of the vein and into the air spaces
(alveoli). This interferes with the exchange ofoxygen and carbon dioxide in the alveoli.
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Extreme shortness of breath, severe difficultbreathing
Feeling of "air hunger" or "drowning"
"Grunting" sounds with breathing
Inability to lie down
Rales
Wheezing
Anxiety
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Restlessness
Cough
Excessive sweating Pale skin
Nasal flaring
Coughing up blood Breathing, absent temporarily
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Listening to the chest with a stethoscope
(auscultation) may show crackles in the
lungs or abnormal heart sounds.
A chest x-ray may show fluid in the lung
space.
An echocardiogram may be performed in
addition to (or instead of) a chest x-ray.
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Blood oxygen levels (low)
A chest X-ray may reveal the following:
Fluid in or around the lung space Enlarged heart
http://www.nlm.nih.gov/medlineplus/ency/article/003804.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003804.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003804.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003804.htm7/30/2019 6 Kuliah Gadar
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An ultrasound of the heart (echocardiogram)
may reveal the following:
Weak heart muscle
Leaking or narrow heart valves
Fluid surrounding the heart
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This is a medical emergency! Do not delaytreatment. Hospitalization and immediatetreatment are required.
Oxygen is given, by a mask or throughendotracheal tube using mechanicalventilation.
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Medications include diuretics such as
furosemide to remove fluid, vasodilators to
help the heart pump better, drugs to treat
anxiety, and other medications to treat theunderlying cardiac disorder.
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Pulmonary edema is a life-threatening
condition. It is often curable with urgent
treatment and subsequent control of the
underlying disorder.
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Long-term dependence on a breathing
machine (ventilator)
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Go to the emergency room or call the local
emergency number (such as 999) if
conditions suggesting pulmonary edema
occur, particularly if breathing is difficult.
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There are currently no publishedguidelines from professional societiesbetween cardiogenic and
noncardiogenic pulmonary edema
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Treatment can be provided while thediagnostic steps are taken begin with a careful history and physical
examination electrocardiogram
measurement of plasma BNP
chest radiograph
transthoracic echocardiogram pulmonary-artery catheter
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In patients with known diseases that can
lead to pulmonary edema, strict compliance
with taking medications in a timely manner
and following an appropriate diet (usually,low in salt) can significantly decrease one's
risk