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non surgical .  NON INVASIV › MEDICAL INVASIV › Surgical .


      Invasive Criteria Complication Prognosis Recovery High cost .

BREATHING . 4. Clinical finding 2. 3. etiology Priority problem ABC  AIR WAY. 5. Look 1. Asses  what’s the problem.1. Anamnesis 2.


Review the causes of acute respiratory failure. 4.     1. Define and classify acute respiratory failure. . 5. Outline management strategies in acute respiratory failure. Describe the pathophysiology of acute respiratory failure. Highlight the clinical presentation of acute respiratory failure. 3. 2.

 acute respiratory failure occurs when: › pulmonary system is no longer able to meet the metabolic demands of the body   hypoxaemic respiratory failure: › PaO2  50 mm Hg when breathing room air hypercapnic respiratory failure: › PaCO2  50 mm Hg. .

7 kPa) .7 kPa) Hypercapnic respiratory failure is defined by a PaCO2 ≥50 torr (≥6.Two basic types of respiratory failure: hypoxemic and hypercapnic Hypoxemic respiratory failure is defined by a room air PaO2 of <50 torr (≥56.

 Depends on › PAO2  FIO2  PACO2  Alveolar pressure  Ventilation › Diffusing capacity › Perfusion › Ventilation-perfusion matching .

 Largely dependent on alveolar ventilation Alveolar ventilatio n  RR x (V .V ) T D  Anatomical deadspace constant but physiological deadspace depends on ventilation-perfusion matching .

Respiratory rate  Tidal volume  Ventilation-perfusion matching  .

FIO2 Ventilation without perfusion (deadspace ventilation) Diffusion abnormality Hypoventilation Normal Perfusion without ventilation (shunting) .

FIO2 Ventilation without perfusion (deadspace ventilation) Diffusion abnormality Hypoventilation Normal Perfusion without ventilation (shunting) .

75% 75% 100% 75% 87.5% .

 Intra-cardiac › Any cause of right to left shunt  eg Fallot’s. Eisenmenger  Intra-pulmonary › Pneumonia › Pulmonary oedema › Atelectasis › Collapse › Pulmonary haemorrhage or contusion .

pneumonia)   Alveolar collapse ( e. chronic bronchitis) Alveoli are filled with fluid ( e.Intra-pulmonary  Small airways occluded ( e.g asthma.g atelectasis) .g pulm edema.

FIO2 Ventilation without perfusion (deadspace ventilation) Diffusion abnormality Hypoventilation Normal Perfusion without ventilation (shunting) .

Dead space ventilation Alveoli that are normally ventilated but poorly perfused Anatomic dead space Gas in the large conducting airways that does not come in contact with the capillaries e.g pharynx .

DSV increase:  Alveolar-capillary interface destroyed e.g emphysema  Blood flow is reduced e.g CHF, PE  Overdistended alveoli e.g positivepressure ventilation


Ventilation without perfusion (deadspace ventilation) Diffusion abnormality


Normal Perfusion without ventilation (shunting)

Less common
Abnormality of the alveolar membrane or a reduction in the number of capillaries resulting in a reduction in alveolar surface area Causes include:
› Acute Respiratory Distress Syndrome › Fibrotic lung disease

FIO2 Ventilation without perfusion (deadspace ventilation) Diffusion abnormality Hypoventilation Normal Perfusion without ventilation (shunting) .

Brainstem Airway Spinal cord Nerve root Lung Nerve Pleura Chest wall Neuromuscular junction Respiratory muscle Sites at which disease may cause ventilatory disturbance .

ARF may occur in a person without previous lung disease or may be superimposed on chronic respiratory failure .Respiratory failure  acute / chronic depending on the duration and the nature of the compensation.

 Mixed  .ARF develops in a variety of clinical settings  primary pulmonary insults  other systemic nonpulmonary disorders  Causes of ARF in adults are often multifactorial.

These disorders primarily interfere with the pulmonary system's ability to adequately oxygenate the blood as it circulates through the alveolar capillaries. .Hypoxemic respiratory failure is seen in patients with acute lung injury (ali) or acute pulmonary edema (cardial / noncardial).

. or  neuromuscular respiratory failure.Hypercapnic respiratory failure is seen in patients with  severe airflow obstruction.  central respiratory failure.

g. aspiration.result of a mismatch of alveolar ventilation and pulmonary perfusion  cause progressive obstruction or atelectasis result in less oxygen being available in distal airways for uptake  blood flow to such abnormal lung units declines  e. pneumonia.. edema. etc  .

inflammation. .Other less common causes of hypoxemia include:  Decreased diffusion of oxygen across the alveolocapillary membrane complex due to interstitial edema.  Alveolar hypoventilation  High altitude. etc.

When gas flow to and from airways remains adequate but blood flow is absolutely or relatively diminished. C02 does not have the opportunity to diffuse from the pulmonary artery blood and C02-rich blood is returned to the left atrium. .

 pulmonary embolus.Increased deadspace ventilation may occur in :  hypovolemia.  poor cardiac output. or  when the regional airway pressure is relatively higher than the regional perfusion pressure produced by the regional pulmonary blood flow .

Several related disease processes often combine and act in concert or synergistically to compound respiratory failure. the patient with chronic pulmonary disease (COPD) and often has associated heart failure (CHF) which increases  worsens hypoxemia . For example.


› the macrophage.ARDS is another type of acute respiratory failure  Increased alveolar capillary permeability in ARDS have centered upon  › the neutrophil. › the pulmonary vascular endothelium and › The cytokine imbalance .

› IL-1.Neutrophil sequestration and migration within the lung remain histologic hallmarks of ARDS  Chemotactic stimuli released within the lung and the activation of neutrophils by circulating mediators :  › TNFa . and › IL-8 .


 There are 5 extremely accurate objective indicators of respiratory distress: › retractions › tachycardia > 130 › pallor/cyanosis › altered mental status › absent breath sounds .

Wheezes  Rales/crackles  Rhonchi/low wheezes  Pleural friction rub  Stridor  Absent!!!  .

    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 .

However.The assessment skills we have discussed so far are the keys to excellent pulmonary assessment. there are several diagnostic tests that may also play a role in these cases:  Pulse Oximeter  Peak flow  ABGs .

 Arterial blood yields information regarding: › acid/base status › ventilation › oxygenation .

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 is long-standing or extremely acute (HCO3) . But first.

35 .45  paCO2 35 .45 torr  paO2 75 .7.100 torr  HCO3 24 .Normal values (room air.35 mEq/L . sea level)  pH 7.

35: acid  > 7. is it acid or base?  < 7. Is it normal or abnormal? › If abnormal. Step 1: Acid/Base Status › Look at the pH. No one has a chronically abnormal pH! .45: base › Write it down! › Note: an abnormal pH is always an acute event.

is it tending toward acid or base?  < 35: base  > 45: acid › Write it down! . Is it normal or abnormal? › If abnormal. Step 2: Respiratory Component › Look at the PaCO2.

increase minute ventilation. . If it is below normal. Step 2: Respiratory Component › Note: the PaCO2 also tells us about ventilation. reduce tidal volume). If it is too high. in most cases minute ventilation should be decreased (slow rate.

is it tending toward acid or base?  < 22: acid  > 26: base › Write it down! . Step 3: Metabolic Component › Look at the HCO3. Is it normal or abnormal? › If abnormal.

acute. Long-standing conditions alter kidney function. Step 3: Metabolic Component › Note: HCO3 also tells us about chronic vs. and will change HCO3. Acute episodes don’t have time to activate the kidneys. . so the HCO3 is normal.

280 ft). . Step 4: Oxygenation › Look at the PaO2. Is it normal or abnormal? › If the PaO2 is below normal (<80 at sea level. don’t get PaO2 values mixed up with your evaluation of acid/base. increase FiO2. Just adjust the oxygen and move on to Step 5…. So.. <65 at 5. › Note: PaO2 has no direct relationship to acid/base status.

› You’ve 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) . and HCO3. › Identify any changes which are consistent with the pH abnormality. PaCO2. Step 5: Put it all together › Look at the pH. They are the cause.

 Oxygen Supplementation › Nasal Cannula › Air-Entrainment Face Masks ("Venturi Masks") › Aerosol Face Mask › Reservoir Face Masks  Noninvasive Positive-Pressure Ventilation .


 Consider NPPV primarily in alert.  Do not use NPPV unless the physician or respiratory care practitioner is familiar with its technical operation.  . and cooperative patients.Do not use NPPV for rapidly deteriorating patients at risk for sudden respiratory arrest. oriented. hemodynamically stable.

Beta2-Agonists  2.Corticosteroids  4.1.Anticholinergic Agents  3.Theophylline preparations  .

RR > 30 menit  Syok  + ventilator mekanik  .Gagal napas .PaCo2 > 60 torr .Ratio Pa O2/FiO2 : < 200 : ARDS < 300 : ALI .


Impairment = Frequency and Intensity of Symptoms and Functional Limitations Symptoms  Nighttime  Need Lung Function awakenings • Spirometry for short-acting β2agonists (SABAs) for quick relief of symptoms days missed  Work/school  Ability • Peak flow to engage in normal daily activities or desired activities assessments  Quality-of-life Adapted from 2007 NHLBI Expert Panel Guidelines (EPR-3). .

progressive decline in lung function.  Likelihood of asthma exacerbations. . or risk of adverse effects from medications Assessment › Frequency and severity of exacerbations › Oral corticosteroid use › Urgent-care visits › Lung function › Noninvasive biomarkers may play an increased role in future Adapted from 2007 NHLBI Expert Panel Guidelines (EPR-3).

.Impairment Well Controlled Symptoms Nighttime awakenings Interference with normal activity Short-acting β2-agonist use for symptom control FEV1 or peak flow ≤ 2 days/week Classification of Asthma Control Not Well Controlled > 2 days/week Very Poorly Controlled Throughout the day ≥ 4/week ≤ 2x/month 1–3/week None Some limitation Extremely limited ≤ 2 days/week > 2 days/week Several times per day < 60% predicted/ personal best > 80% predicted/ personal best 60–80% predicted/ personal best Patients ≥ 12 years of age Adapted from 2007 NHLBI Expert Panel Guidelines (EPR-3).

Bagan Terapi Asma Saat Ini Pengontrol (Controller) Pelega (Reliever) Tingkat 4: PERSISTEN BERAT Terapi harian multi obat •Steroid inhalasi (ICS) •Long Acting 2 -agonist (LABA) •Oral steroid Turunkan dosis ketika terkontrol Inhalasi 2-agonis prn Menghindari faktor pencetus Tingkat 3: PERSISTEN SEDANG Terapi harian •Steroid inhalasi (ICS) •Long Acting 2 -agonist (LABA) Inhalasi 2-agonis prn Menghindari faktor pencetus Tingkat 2: PERSISTEN RINGAN Terapi harian •Steroid inhalasi (ICS) • Penyesuaian dosis setelah 3 bulan terkontrol • harus tetap dimonitor/evaluasi Inhalasi 2-agonis prn Menghindari faktor pencetus Tingkat 1: INTERMITEN Tidak perlu Inhalasi 2-agonis prn Menghindari faktor pencetus Naikkan dosis jika tidak terkontrol .

Important elements include: › A written action plan  Guides › Recognition of early signs of worsening asthma patient self-management of exacerbations at home  Especially important for patients with moderate-to-severe persistent asthma and any patient with a history of severe exacerbations . Early treatment is best.

or deterioration in symptoms or peak  Decreased  Decreased responsiveness to inhaled beta2-agonists. or duration of beta2-agonist effect .› › Appropriate intensification of therapy Prompt communication between patient and clinician about:  Serious flow.

 Inhaled beta2-agonist to provide prompt relief of airflow obstruction Systemic corticosteroids to suppress and reverse airway inflammation › ›  For moderate-to-severe exacerbations. or For patients who fail to respond promptly and completely to an inhaled beta2agonist .

    Past history of sudden severe exacerbations Prior intubation or admission to ICU for asthma Two or more hospitalizations for asthma in the past year Three or more ED visits for asthma in the past year .

 Hospitalization or an ED visit for asthma in the past month Use of >2 canisters per month of inhaled short-acting beta2-agonist   Current use of systemic corticosteroids or recent withdrawal from systemic corticosteroids .

   Difficulty perceiving airflow obstruction or its severity Comorbidity. as from cardiovascular diseases or chronic obstructive pulmonary disease Serious psychiatric disease or psychosocial problems .

 Low socioeconomic status and urban residence Illicit drug use   Sensitivity to Alternaria .

especially those Moderate-to-severe persistent asthma or History of severe exacerbations . Develop each with: › › a written action plan with patient.

 The plan should include: › Signs. and peak flow levels that indicate deteriorating asthma How to adjust medications in response to deteriorating asthma When to seek medical help Emergency phone numbers › › › . symptoms.

 Use inhaled short-acting beta2-agonist: › Up to three treatments of 2 to 4 puffs by inhaler at 20-minute intervals Single nebulizer treatment OR ›  Assess symptoms and/or peak flow after 1 hour .

or chest tightness and Response to beta2-agonist sustained for 4 hours  . shortness of breath. Peak flow >80% predicted or personal best and/or  No wheezing. cough.

double dose for 7 to 10 days Contact clinician within 48 hours for instructions  . May continue 2 to 4 puffs beta2-agonist every 3 to 4 hours for 24 to 48 hours PRN  For patients on inhaled corticosteroids.

 Peak flow 50% to 80% predicted or personal best or Persistent wheezing. or chest tightness  . cough. shortness of breath.

 

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 and peak flow are stable
Contact clinician urgently (same day) for instructions

Peak flow <50% predicted or personal best, or
Marked wheezing, shortness of breath, cough, or chest tightness, or Distress is severe and nonresponsive, or

Response to beta2-agonist lasts <2 hours

IMMEDIATELY  Take up to three treatments of 4 to 6 puffs beta2-agonist every 20 minutes PRN  Start oral corticosteroid  Contact clinician  Go to emergency department or call ambulance or 9-1-1

   Correction of significant hypoxemia Rapid reversal of airflow obstruction Reduction of likelihood of recurrence .

provided there is improvement .• FEV1 or PEF 50% to 80% predicted or personal best • Physical exam: moderate symptoms • Inhaled short-acting beta2-agonist every 60 minutes • Systemic corticosteroid • Continue treatment 1 to 3 hours.

accessory muscle use.• FEV1 or PEF <50% predicted or personal best • Physical exam: severe symptoms at rest. chest retraction • History: high-risk patient • No improvement after initial treatment • Oxygen • Inhaled short-acting beta2-agonist hourly or continuously + inhaled anticholinergic • Systemic corticosteroid .

• FEV1 or PEF >70% • Response sustained 60 minutes after last treatment • No distress • Physical exam: normal • Discharge Home .

• FEV1 or PEF >50% but <70% • Mild-to-moderate symptoms • Individualized decision re: hospitalization .

• FEV1 or PEF <50% • PCO2 >42 mm Hg • Physical exam: symptoms severe. drowsiness. confusion • Admit to hospital intensive care .

• Inhaled beta2-agonist hourly or continuously + inhaled anticholinergic • IV corticosteroid • Oxygen • Possible intubation and mechanical ventilation • Admit to hospital ward .

reduce therapy Monitor -Theophylline-SR -Leukotriene -Long-acting inhaled β2.agonist -Oral corticosteroid  Reliever: Rapid-acting inhaled β2-agonist prn STEP Down .Step Up dan Step Down Therapy of Asthma Outcome: Asthma Control Outcome: Best Possible Results Controller:  Controller: Controller: None  Controller: Daily inhaled corticosteroid    Daily inhaled corticosteroid Daily longacting inhaled β2-agonist  Daily inhaled corticosteroid Daily long – acting inhaled β2-agonist plus (if needed)  When asthma is controlled.








his temperature 37.A 62-year-old man presents with a threeday history of progressive dyspnea.9 degreesC. his heart rate 110 beats per minute. and low-grade fever  Congestive heart failure history  His blood pressure is 95/55 mm Hg. and his oxygen saturation while breathing ambient air 86 percent  . nonproductive cough.

Chest auscultation reveals rales and rhonchi bilaterally  A chest radiograph shows bilateral pulmonary infiltrates consistent with pulmonary edema and borderline enlargement of the cardiac silhouette  How should this patient be evaluated to establish the cause of the acute pulmonary edema and to determine appropriate therapy  .

This results from malfunctioning of the heart. . Pulmonary edema is a condition characterized by fluid accumulation in the lungs caused by back pressure in the lung veins.

or other disorders characterized by cardiac dysfunction. Pulmonary edema is a complication of a myocardial infarction (heart attack). cardiomyopathy. mitral or aortic valve disease. .

Increased pressure in these veins forces fluid out of the vein and into the air spaces (alveoli). This interferes with the exchange of oxygen and carbon dioxide in the alveoli. Fluid backs up into the veins of the lungs. .

severe difficult breathing  Feeling of "air hunger" or "drowning"  "Grunting" sounds with breathing  Inability to lie down  Rales  Wheezing  Anxiety  .Extreme shortness of breath.

Restlessness  Cough  Excessive sweating  Pale skin  Nasal flaring  Coughing up blood  Breathing. absent temporarily  .

 An echocardiogram may be performed in addition to (or instead of) a chest x-ray.  .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.

 Blood oxygen levels (low)  A chest X-ray may reveal the following:  Fluid in or around the lung space  Enlarged heart .

 An ultrasound of the heart (echocardiogram) may reveal the following:  Weak heart muscle  Leaking or narrow heart valves  Fluid surrounding the heart .

 Oxygen is given. Hospitalization and immediate treatment are required. by a mask or through endotracheal tube using mechanical ventilation.This is a medical emergency! Do not delay treatment.  .

vasodilators to help the heart pump better. . Medications include diuretics such as furosemide to remove fluid. drugs to treat anxiety. and other medications to treat the underlying cardiac disorder.

 Pulmonary edema is a life-threatening condition. . It is often curable with urgent treatment and subsequent control of the underlying disorder.

 Long-term dependence on a breathing machine (ventilator) .

particularly if breathing is difficult. . Go to the emergency room or call the local emergency number (such as 999) if conditions suggesting pulmonary edema occur.

 There are currently no published guidelines from professional societies between cardiogenic and noncardiogenic pulmonary edema .


 Treatment can be provided while the diagnostic steps are taken › begin with a careful history and physical › › › › › examination electrocardiogram measurement of plasma BNP chest radiograph transthoracic echocardiogram pulmonary-artery catheter .

low in salt) can significantly decrease one's risk . strict compliance with taking medications in a timely manner and following an appropriate diet (usually. In patients with known diseases that can lead to pulmonary edema.

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