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Diagnosis and Management of Acute Respiratory Failure (ARF)

Dr. Prabowo Wicaksono Y.P., SpAn

Department of Anesthesiology

UNISSULA Medical Faculty/ RSI Sultan Agung

Semarang

2007


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I. DEFINITION/ CLASSIFICATION OF ARF

ARF : One of the most common disorders leading to ICU admission

Occurs when pulmonary systems is no longer able to meet the metabolicdemand of the body.

Pulmonary system : 2 metabolic roles:

- Oxygenation of arterial blood

- Elimination of CO 2

Two basic types of RF:

TYPE I : Hypoxemic . Interference with the pulmonary systemss ability toadequately oxygenate the blood as is circulates through the alveolar

capillaries. PaO 2 (room air) < 60 mmHg. (Normal PaO 2: 75-100 mmHg). TYPE II : Hypercapnic . Failure to prevent CO2 retention (e.g., severeairflow obstruction, central resp. failure, neuromuscular resp. failure)PaCO 2 > 50 mmHg. (Normal PaCO 2: 35-45 mmHg)


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II. CAUSES OF ARF

RF may results from primary pulmonary insults and from other systemicnonpulmonary disorders (CNS, CV, neuromuscular systems, upper and lower

airways, pulmonary parenchyma). Often multifactorial.CAUSES OF RESPIRATORY FAILURE

Disorders associated with Abnormal Oxygen Onloading (Hypoxemic RF)

Lower Airway and Parenchyma

NEOPLASM TRAUMA (pulmo. contusion, laseration ARDS

INFECTION OTHER (Broncospasm, CHF) Interstitial lung disease

Pulmonary emboli

Atelectasis

Cystic fibrosis

Disorders associated with Inadequate CO2 Offloading (Hypercapneic RF)

BRAIN : Drugs (opioids, benzodiazepines, propofol, barbiturates, GA, poisons)

Metabolic (e.g.Hyperglycemia, hypocalcemia)

Neoplasma, Infection, Increased ICP.

NERVES AND MUSCLES: trauma, metabolic, drugs, poisons, neoplasm, infection


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UPPER AIRWAY: Tissue enlargement, infenction, trauma.

CHEST BELLOWS: trauma (rib fractures, flail chest), other contributing factors (e.g.obesity,ascites, spondylitis)

III. PATHOPHYSIOLOGY OF ACUTE RESPIRATORY FAILUREA. HYPOXEMIA

The underlying physiologic abberation in hypoxemic RF is usually the resultsof a mismatch of alveolar ventilation and pulmonary perfusion . Diseasesprocesses that cause progressive obstruction or atelectasis (e.g. pneumonia,aspiration, edema) results in decrease in the amount of oxygen available indistal airways for uptake .

This mismatch of ventilation (V) and perfusion (Q) wherein perfusion isrelatively greater than ventilation to a given lung unit is called shunt effect .The venous blood entering pulmonary capillaries acts as if did not travel to

the lung at all because it remains relatively poorly oxygenated as it returns tothe left atrium , the physiologic effect of this type of V/Q mismatch ishypoxemia.

Treatment should be directed toward removing obstruction, reopeningatelectasis zones, and preventing closure of the affected lung units.

The most likely reason for a patient to be hypoxemic is this type of V/Qmismatch.


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ALVEOLUS

PULMONARYCAPILLARY

FREE AIR:

PiO2 : 20.9 % x 760 = 159 mmHg

PiCO2 : 0.04 % x 760 = 0.3 mmHg

PiN2 : 78.6 % x 760 = 597mmHg

PiH2O : 0.46 % x 760 = 3.5 mmHg N2 H2O

O2

PAO2:104 mmHg

CO2

PACO2:40 mmHg

O2PaO2:40 mmHg

O2

PaO2:104 mmHg

CO2PaCO2:45 mmHg

CO2PaCO2:40 mmHg

DIFUSSIONPROCESS

PAN2:573 mmHg

PAH2O:47 mmHg


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B. HYPERCAPNIA

Hypercapnia RF is caused by one or more factors describes in equation foalveolar minute ventilation:

VA= (VT-VD) . f VA : minute alveolar ventilation

VT : tidal volume

VD : physiologic dead space (alveolus is well ventilted but poorly perfused)

f : respiration frequencyHypercapnia may results from decreased VT or f as occurs with drug ingestion,anestesia, change in medullary center for respiration, fatigue. An elevatedPaCO 2 normally increases ventilatory drive. Therefore, hypercapnic respiratoryfailure may also imply that the patient is:

- Unable to sense the elevated PaCO 2 due to drug, alkalemia, COPD, etc- Unable to neurologically signal the effector mechanism of ventilation becauseof spinal cord injury, neuromuscular blockade, Guillan- Barre synd, MyasteniaGravis.

- Unable to effect a response from the muscle of respiration because of fatigue,malnutrition etc.


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Tratment of decrease VT or respiration rate may require special medications(e.g. for Myastenia), reversal of sedation or other drugs, intubation/ mechanicalventilation to rest fatigued muscles, nutrition, resp. stimulant and as alwaystreatment of other possible primary cause.

Increased physiologic dead space (VD) may also produce hypercapnia andrepresents the other type of V/Q mismatch. When gas flow to and from airwaysremain adequate but blood flow is absolutely or relatively diminished, CO 2 doesnot have the opportunity to diffuse from the pulmonary artery blood, and CO 2 rich blood is returned to the left atrium. This condition may occur in

hypovolemia, pulmonary embolus, poor cardiac output.IV. MANIFESTATIONS OF ARF

Clinical manifestations of respiratory distress commonly reflect signs andsymptoms of hypoxemia, hypercapnia, or both. These include:

-Altered mental status, ranging from agitation to somnolence.-Evidence of increased work of breathing (i.e., nasal flaring, use of accessorymuscles, intercostal/suprasternal/supraclavicular retraction, tachypnea,hyperpnea, or a paradoxical breathing pattern)

- Bradypnea


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- Cyanosis of mucosal membranes (e.g., tongue, mouth) or nail beds.

- Diaphoresis, tachycardia, hypertension, and other sign of catecolamine release.

Laboratory test :- A key test is the arterial blood gas (PaO 2 and PaCO 2, to differentiate between

ARF type I and II )

- Additional test: electrolytes, drug level : clue to underlying etiology of ARF

- A chest radiograph: pumonary infiltrates: a hypoxemic component for ARF, aclear lung fields suggest possible hypercapnic RF, although considerable overlapexists.


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MANAGEMENT

1. Clear the airway

2. Oxygen supplementation

3. Noninvasive positive pressure ventilation

4. Tracheal intubation and mechanical ventilation

5. Pharmacologic adjuncts


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PRIMARY SURVEYAirway : Open the airwayBreathing : Provide positive-pressure

ventilationCirculation : Give chest compressionsDefibrillation : Shock VF / pulseless VT

Airway : Establish advanced airway

control Perform endotracheal

intubationBreathing : Assess the adequacy of

ventilation via endotrachealtube

Provide positive-pressure

ventilationsCirculation : Obtain iv access Continue CPR Provide rhythm cv

Differential Diagnosis

SECONDARY SURVEY1. CLEAR THE AIRWAY


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Airway obstruction causedinadequate ventilation although thepatient breathing sontaneously. Thecaused of obstruction:

Tongue, epiglottisForeign object

LIDAHOBSTRUKSI AIRWAY

AIRWAY OBSTRUCTION


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PRIMARY PRIORITY: CLEAR THE AIRWAY

Manual: Triple airway maneuver: - Head Tilt

- Chin lift

- Jaw Thrust Airways : - Oropharyngeal airways (Guedel)

- Nasopharyngeal airways- Laryngeal mask airway

Endotracheal Intubation


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HEAD TILT CHIN LIFTCAUTIONS !!! CERVICALTRAUMA ??


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JAW THRUST


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Oropharyngeal Airway

To prevent obstruction of hypofaring by the tongue

To facilitate suctionTo prevent tongue or ETT

bite

Unconscious patientwithout gag reflect.


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Oropharyngeal Airway/Guedel


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Measure the right size of Oropharyngeal airway/Guedel

Complication :Total obstructionLaringospasmVomit


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Oropharyngeal airway

How to insert correctly


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Nasopharyngeal Airway

Indication:- Spontaneous breathing, unconscious patient.- Better tolerated than OPA


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Nasopharyngeal Airway

Complication Nasal mocous damaged

Laryngospasme


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How to insert Nasophryngeal Airway1.

2. 3.


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LARYNGEAL MASK AIRWAY

Very useful in difficult intubation situation


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Tracheal Intubation

- Gold standart in airway management.- Not easy to perform, complication can be serious

- Skill, experience and training are essential to minimaze complication


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Clear and secure airwayReduced aspiration risk To fasicilitate intra tracheal suctionTo fasicilitate high concentration oxygensupport

Advantages of Tracheal Intubation


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HipoxiaTrauma

Vomiting, aspirationHipertension, dysritmiaOne lung intubationOesophageal intubation

Bradycardia, vagal reflexCardiac arrest

Complication of tracheal intubation


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TRACHEAL INTUBATION EQUIPMENT


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Oral intubation technique

1

2


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VISUALIZATION OF THE CORD

VOCAL CORD: MUST SEE THIS WHEN INTUBATE !!!

TRAKEA


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BURP MANUEVER To aid visualization of the cordPush the cricoid cartilage back, up and right (BURP)

BURP

THYROID

CRICOID

ADAMS APPLE


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3

4


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5


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Nasal Intubation technique

1 2


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3

4


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5


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TRAI NI NG I S ESSENT I AL


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Skilled trained personnel

Complete intubation equipmentPerformed less than 30 secondsPerform BURP Manuever Use high volume low pressure cuff ETT

Measures to prevent complication of trachealintubation


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MANUAL POSITIVE PRESSURE VENTILATION WITHETT


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2. Oxygen supplementationMost patient with ARF require supplemental oxygen. Oxygen transfer fromalveolar gas to capillary blood occurs by diffusion through alveolar-capillarymembrane, which driven by te oxygen partial pressure gradient between thePAO 2 (alveolus) and the PaO 2 (arterial blood) of the pulmonary capillaryblood. In most cases, the PAO 2 can be substantially increased by use of supplemental oxygen, thus increasing the gradient across the membrane andimproving PaO 2. This should be considered a temporizing intervention while

the primary etiology of hypoxemia is diagnosed and treated.The effectiveness of each oxygen supplement devices is determined by thecapacity of the device to deliver sufficient oxygen at high enough flow rate tomatch the patients spontaneous inspiratory flow rate.

Any entrained room air (FiO 2 = 0.21) will dilute (decrease) the FiO 2 of the

delivered gas in such a way that the tracheal FiO 2, and hence PAO 2 may beconsiderably lower than the FiO 2 delivered from the oxygen source.


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Oxygen supplement systyem are classified as :1. Low oxygen, low flow devices e.g. nasal cannula2. Controlled oxygen, high flow devices e.g. venturi mask3. Variable oxygen, moderate flow devices e.g. aerosol face mask4. High oxygen, high flow devices e.g. reservoir face mask, Resuscitation Bag

Mask-Valve Unit.

1. Nasal CannulaShort prongs of the nasal cannula are inserted intothe nares. Oxygen (100%) is delivered throughcannula, but at low flow rates (0.5-5 L/min).The maximal tracheal FiO 2 is 0.40 - 0.50 (40-50%).Higher flow rates do not result in much higher FIO 2 levels and have drying and irritating effect on nasalmucosa. Comfortable and well tolerated by many

ARF patient in whom precise control of FiO 2 is notnecessary.


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Flow (L/men) Desired FiO 2Measured FiO 2

Gibson et al Schachter et al

1 0.24 0.22 0.23

2 0.28 0.21 0.22 0.24

3 0.32 0.22 0.24 0.25

4 0.36 0.26

5 0.40 0.24 0.25

10 0.52 0.30 0.46

15 0.56 0.35 0.61

NASAL CANNULA


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Gas flow (L/men) FiO2

4 8 0.24 / 0.28 / 0.35 / 0.40 /0.50 / 0.60

VENTURI MASK

3 A l F M k


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3. Aerosol Face MaskThe mask with large side holes is attached by large-bore tubing to a nebulizer, which blends 100%oxygen and room air to deliver gas at a preset FiO 2 level. Flow matching can be evaluated by observingthe patient during spontaneous breathing. If theentire aerosol mist dissappears from mask duringinhalation, the patients inspiratory flow demands areprobably exceeding the capacity of nebulizer.

4. Reservoir Face MaskIncorporates a reservoir bag with the face mask fromwhich the patients breathes. The reservoir bag is

filled from the 100% oxygen supply source. The flowrate of oxygen is adjusted so that bag remainscompletely or partially distended throughout therespiratory cycle. FiO2: 0.6-0.9 (60-90%).


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Flow (L/men) Desired FiO 2

5 -6 0.46 7 0.57 8 0.6

SIMPLE FACE MASK

Flow (L/men) Desired FiO 26 0.6

7 0.7

8 0.8

9 -10 0.9 0.99

RESERVOIR FACE MASK


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3. NONINVASIVE POSITIVE PRESSUREVENTILATION

NPPV provides ventilatory assistance,controlled FiO 2 and positive airwaypressure without invasive artificialairway, thus avoids meany of thecomplication associated with intubationand mechanical ventilation.

Two form of NPPV: CPAP (ContinuousPositive Airway Pressure) and BIPAP(Bilevel Positive Airway Pressure).

CPAP: functionally equivalent to PEEP which delireved by a mechanicalventilator through face mask instead of ETT.

BIPAP: Combination of PSV (Pressure Support Ventilation) and CPAP

Best utilized in the alert, cooperative patient whose respiratory condition isexpected to improve in 48-72 hours, e.g. acute exacerbations of COPD.


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4. TRACHEAL INTUBATION ANDMECHANICAL VENTILATION

TUJUAN KLINIS / INDIKASI PEMAKAIANTUJUAN KLINIS / INDIKASI PEMAKAIANVENTILASI MEKANIKVENTILASI MEKANIK

GAGAL NAFAS HIPOKSEMIK :

R ev er s e h y p o x em i a dgn pemberian PEEP dan konsentrasi O2tinggi (ARDS,edema paru atau pneumonia akut)

GAGAL NAFAS VENTILASI:

R ev er s e ac u t e r e s p i ra t o r y a c i d o s is

- Koma : trauma kepala, encefalitis, overdosis, CPR- Trauma med spinalis, polio, motor neuron disease

- Polineuropati, miastenia gravis

- Anesthesia (relaksan u/operasi, tetanus, epilepsi)

STABILISASI DINDING DADA:

F l ai l c h es t

MENCEGAH ATAU MENGOBATI ATELEKTASIS


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Kriteria tradisional untuk bantuan ventilasi mekanikKriteria tradisional untuk bantuan ventilasi mekanik

35-45> 60Ventilasi (PaCO2-

mmHg)

25-65(FiO2 1.0)> 350P(A-aDO2) mmHg

75-100 (air) 35x/mMekanik (RR)

NORMAL RANGEINDIKASI VENTILASIPARAMETER


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5. PHARMACOLOGIC ADJUNCTSMany disease causing ARF produce similar anatomic and physiologicderangements, incluiding bronchial inflammation, mucosal edema, smooth

muscle contraction, and increased mucos production and viscosity. Each of these processes may contribute to obstruction of airway gas flow, increasedairway resistance, V/Q mismatch, and elevated VD. Some pharmacologicagents have proven helpful in the care of such patients and may directly alter the shunt or dead space effect.

1. 2 AgonistsInhaled 2 agonists (e.g. Albuterol, Terbutaline, Metoproterenol sulfate )stimulate 2-adrenergic receptor causes bronchial and vascular smoothmuscle relaxation.

2. Anticholinergic agents

Ipratropium bromide competes with acetylcholine at bronchial receptor site,causing an increase in intracellular cGMP, signaling bronchial smooth musclerelaxation.


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3. Corticosteroids

The central role of inflammation in obstructive airway disease is established, andthe benefit from aggressiv corticosteroid use in ashmatic patient with ARF is well

documented.4. Antibiotics

Bacterial infection (bronchitis/ pneumonia) frequently precipitates ARF. Antibioticsshoud be used when there is clinical suspicion that bacterial pulmonary infectionis present (e.g., change in sputum characteristics, pulmonary infiltrates on chst

radiograph, fever, leukocytosis)


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