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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



Perfusionwithout


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



Perfusionwithout


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



Perfusionwithout


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



Perfusionwithout


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



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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


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




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
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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

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