pemicu 4 meidy.pptx

8/11/2019 pemicu 4 meidy.pptx

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Meidy 4


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RESPIRATORY FAILURE Ketidakmampuan paru-paru untuk memenuhi

tuntutan metabolisme tubuh. Ini dapat dari

kegagalan oksigenasi jaringan dan / ataukegagalan homeostasis CO2


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RESPIRATORY FAILURE

Definisi Respirasi adalah pertukaran gas antara

organisme dan lingkungannya. Fungsi sistem

pernapasan adalah untuk mentransfer O2 dari

atmosfer ke darah dan menghilangkan CO2 daridarah.

Kegagalan klinis pernapasan didefinisikan sebagai

PaO2 50 mmHg.


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Respiratory system includes:

CNS (medulla)Peripheral nervous system (phrenic nerve)Respiratory muscles

Chest wallLungUpper airwayBronchial tree

AlveoliPulmonary vasculature


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Clinical Manifestation

Hypercapnia

somnolence

lethargy

coma

asterikscan not be quiet

tremor

garbled speech

headache

papil edema

Hypoxemia

anxiety

tachycardia

tachypnea

diaphoresisarrhythmias

change in mental status

confused

cyanosis

hypertension

hypotension

convulsions

lactic acidosis


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Cause of respiratory failure

A. Extrinsic lung disorders

1. The emphasis of the respiratory center

- An overdose of the drug (narcotic

sedative)

- Trauma cerebral or myocardial

- Poliomyelitis bulbar

- Encephalitis


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2. Neuromuscular disorders

- Cervical spinal injury

- Guillan barre syndrome

- Amiotrofik lateral sclerosis

- Miatenia gravis

- Muscular dystrophy3. Pleura and chest wall disorders

-Chest Injury

-pneumothorax- Pleural effusion

-Kifoskoliosis

-Obesity: pickwickan Syndrome


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B. Intrinsic Pulmonary Disorder

1. Diffuse obstructive disorders

a. Emphysema, COPD

b.Asma, status asthmaticus

c. cystic fibrosis

2. Restrictive lung disorders

a. Interstitial fibrosis due to various reasons

b. sarcoidosis

c. scleroderma

d. pulmonary edema

e. Ateletaksis

f. pneumonia consolidation3. Pulmonary vascular disorders

a. pulmonary embolism

b. severe emphysema


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RESPIRATORY FAILURE

HYPERCAPNIC HYPOXEMIC

ACUTE CHRONIC ACUTE CHRONIC

CLASSIFICATION


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Hypoxemia (Type 1)


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PATHOPHYSIOLOGY

Hipoksia adalah pengiriman oksigen yang

tidak memadai ke jaringan dan disebabkan

oleh salah satu dari lima mekanisme yang

berbeda. Hipoksia secara sewenang-wenang

didefinisikan sebagai PaO2 60 mmHg.

Hipoventilasi: Meningkatnya PaCO2

menggantikan oksigen dari alveolus,menurunkan PaO2 dan mengurangi gradien

difusi O2 melintasi membran paru


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Right-to-left shunting: Unoxygenated blood

enters the systemic circulation. This may occur

secondary to perfusion of underventilated

lung or with congenital heart anomalies.

Ventilation/perfusion mismatch: Results from

regional alterations of ventilation or

perfusion.

Diffusion impairment: Caused by impairment

of the alveolar blood barrier.

Low FiO2: The cause of high-altitude hypoxia


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PATHOPHYSIOLOGY

HYPOXEMIA

Decreased PIO2or fraction

Hypoventilation

Impaired diffusion

Shunt

V/Q mismatch


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CLINICAL FEATURES

Signs and symptoms are nonspecific, rangingfrom tachycardia and tachypnea to centralnervous system (CNS) manifestations such as

agitation, seizures, and coma. At PaO2 20 mmHg, there is a paradoxical

depression of the respiratory drive.

Dyspnea mungkin saja atau mungkin tidakhadir, dan sianosis merupakan indikatorsensitif dari PaO2 status.


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DIAGNOSIS AND DIFFERENTIAL

Pulse oximetry is a useful screening test, but

arterial blood gas analysis defines the

diagnosis.

pemeriksaan tambahan serupa digunakan

untuk menentukan penyebab dyspnea

mungkin menjelaskan kelainan yang

menyebabkan hipoksia.


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EMERGENCY DEPARTMENT CARE AND

DISPOSITION

Hipoksia diperlakukan sama seperti dyspnea,

dukungan, mengidentifikasi, dan agresif

mengobati gangguan yang mendasari,

berusaha mempertahankan PaO2 60 mmHg.

Semua pasien dengan hipoksia persisten

memerlukan rawat inap sampai kelainan

memadai dan stabil. Sampel darah arterisering mungkin memerlukan garis arteri.


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Hypercapnia (Type 2)


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PATHOPHYSIOLOGY

didefinisikan sebagai 45 mmHg PaCO2 dandisebabkan oleh hipoventilasi. Hal ini hampirtidak pernah disebabkan oleh penyakit paru-paru

intrinsik atau peningkatan produksi CO2. Menit ventilasi tergantung pada laju pernapasan

dan volume tidal; menurun aku baik akanmenyebabkan hipoventilasi.

Gangguan yang menyebabkan hipoventilasi danhiperkapnia bervariasi, tetapi efeknya selaludapat ditelusuri hubungan menit ventila


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Alveolar ventilation is less than minute

ventilation; although this term is moreappropriately used in describing ventilation,

alveolar ventilation is impractical to measure. Ventilasi alveolar kurang dari satu menit

ventilasi, meskipun istilah ini lebih tepatdigunakan dalam menggambarkan ventilasi,ventilasi alveolar tidak praktis untukmengukur.


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Kedua parameter di menit ventilasi

dikendalikan melalui keluaran saraf eferen dari

kemoreseptor di medula.


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CLINICAL FEATURES

Signs and symptoms of hypercapnia aredependent on the rate and degree of elevation.Acute rises are associated with an increase in

intracranial pressure, confusion, lethargy,seizures, and coma. On physical exam, asterixismay also be found.

Acute changes to PaCO2 100 mmHg may lead to

cardiovascular collapse. In acute retention, foreach 10-mmHg ncrease of PaCO2 , the pH willdecrease 0.1 U.


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Chronic changes in PaCO2 may be well

tolerated. To maintain a neutral milieu, the

kidneys retain [HCO3]. In the chronic setting,

for every 10 mmHg of PaCO2 over 40 mmHg,[HCO3 ] increases 3.5 meq/L.


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DIAGNOSIS AND DIFFERENTIAL

Given clinical suspicion, the diagnosis will be

confirmed

on arterial blood gas analysis. See Table

32-2 for further differential diagnosis.


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EMERGENCY DEPARTMENT CARE


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EMERGENCY DEPARTMENT CARE

AND DISPOSITION

Hiperkapnia diperlakukan dengan cara yang samasebagai hipoksia: mengidentifikasi ancamanterhadap kehidupan, mengevaluasi dan agresifmengobati kekurangan dalam ABC.

Identifikasi etiologi yang mendasari akanmemungkinkan pengobatan terfokus.

Sebagai contoh, dosis narkotika menyebabkandepresi pernafasan akan menanggapi nalokson,

sementara ventilasi tidak efektif sekunder untukkelemahan otot pernafasan akan meresponhanya untuk ventilasi dibantu atau mekanis.


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Oksigen tambahan harus diberikan untuk

mempertahankan tingkat yang dianggap

normal untuk pasien. Oksigen tidak harus

ditahan berdasarkan khawatir'' penurunanritme pernafasan.'' Hipoksia akan membunuh

pasien, sementara hanya hiperkapnia ekstrim

akan melakukan hal yang sama.


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BiPAP or CPAP may be used as a bridge until a

definitive diagnosis of hypercapnia and a

treatment plan can be made, but it is never a

longterm option. If all else fails, mechanicalventilation is indicated.

Disposition depends on the underlying cause

and frequently requires admission to amonitored bed.


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Respiratory Failure : Medication

Farmakoterapi adalah untuk edema paru

kardiogenik dan eksaserbasi akut PPOK

Tujuan terapi edema paru kardiogenik:

mencapai tekanan kapiler paru irisan 15-18

mm Hg dan indeks jantung lebih besar dari 2,2

L/min/m2while mempertahankan tekanan

darah adekuat dan perfusi organ


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Furosemide : IV

Metolazone: sebagai terapi tambahan padapasien awalnya refrakter terhadap

furosemide dan digunakan dalam kombinasi

dengan furosemide untuk diuresis lebihagresif

Diuretics : 1stline


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Mengurangi kebutuhan oksigen miokard

dengan menurunkan preload dan afterload Nitrogliserin sublingual: berguna dalam

pasien yang datang dengan edema paru akut

dengan tekanan darah sistolik paling sedikit100 mm Hg

Nitrates


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Topical: wajar pada pasien menyajikan

dengan kelas I-II CHF IV: Tanda-tanda parah edema paru atau HF

Nitroprusside natrium: menghasilkan

vasodilatasi vena dan sirkulasi arteri, Padadosis yang lebih tinggi, hal itu mungkin

memperburuk iskemia miokard dengan HR

Nitrates


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Morphine IV is an excellent adjunct in the

management of acute pulmonary edema Venodilation : reduces preload

Arterial dilatation : reduces systemic vascular

resistance and may increase cardiac output

Opioid Analgesics


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Dopamine : Lower doses : stimulate mainly dopaminergic

receptors that produce renal and mesentericvasodilation

Higher doses : produce cardiac stimulation and renalvasodilation

Doses of 2-10 g/kg/min

tachycardia, ischemia,dysrhythmias

Doses > 10 g/kg/min vasoconstrictionafterload

Inotropic Agents


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Norepinephrine :

used in protracted hypotension after adequatefluid replacement

It stimulates beta1- and alpha-adrenergic

receptors cardiac muscle contractility & HR

SBP & CO

Adjust and maintain infusion to stabilize BP

Inotropic Agents


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Dobutamine :

produces vasodilation and increases the inotropicstate

At higher dosages heart rates

exacerbating myocardial ischemia

Inotropic Agents


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Terbutaline : relax bronchial smooth muscle,

relieving bronchospasm and reducing airwayresistance

Albuterol : relaxation of bronchial smooth

muscle

relieves bronchospasm and reducesairway resistance

Beta2 Agonists


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Effective in accelerating recovery from acute

COPD exacerbations and are an importantanti-inflammatory therapy in asthma

Corticosteroids


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Pneumothorax

Pneumotoraks - udaraberada di antara paru-parudan dinding dada dan paru-paru runtuh.

Biasanya, dua lapisan tipisdari jaringan (pleura)memisahkan paru-paru dandinding dada.

Setiap udara yang bocor kedalam ruang ini (ruangpleura) akan menyebabkanparu-paru colaap


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Normal Physiology

Chest Wall

Pleura

Pleural Space

Diaphragm


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Pneumothorax

Signs and symptoms

of a pneumothorax

include:

Tiba-tiba, nyeri dada

yang tajam

Sesak napas

dada sesak nadi cepat

Cepat, napas pendek


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Clasification

Pneumothorax

Etiology

SpontaneousPneumothorax

Primary

Secondary

Traumatic

Non-Iatrogenic

Iatrogenic

Type of Fistula

SimplePneumothorax

OpenPneumothorax

TensionPneumothorax


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Spontaneous Pneumothorax

Primary Spontaneous Pneumothorax (PSP)

Pneumothorax occurs without a history of

underlying lung disease before Attack : the healthy person, young adult, heavy

physical activity, but at rest

Secondary Spontaneous Pneumothorax (SSP)

Peumothorax due to underlying lung disease (TB,COPD, bronchial asthma, pneumonia, lung tumors)


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Traumatic Pneumothorax

Penetrating trauma or notruptur of thepleura, chest wall, lung

Non-Iatrogenic Traumatic Pneumothorax Injury due to accident (injury of chest wall

open-close, barotrauma)

Iatrogenic Traumatic Pneumothorax

Accidental

Artificial/deliberate


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Iatrogenic Traumatic Pneumothorax

Accidental

Due to medical treatmenterrors /

complications the action (paresthesias chest,pleural biopsy, etc)

Artificial

Deliberatefilling air into the pleural cavitythrough a needle with a Maxwell Box (TBtherapy before AB)


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Pathology

Pneumothorax

Closed

pneumothorax

Open

pneumothorax

Tension

pneumothorax


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Closed

pneumothorax

Open

pneumothorax

Tension

pneumothorax

The pleural tear

Is sealed

The pleural tear

is open

The pleural tear

act as a ball &

valve mechanism

The pleural

cavity pressure

is < theatmospheric

pressure

The pleural

cavity pressure

is = theatmospheric

pressure

The pleural cavity

pressure is > the

atmosphericpressure


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Physical Examination

pasien dengan pneumotoraks dapat berkisar darisepenuhnya bergejala hingga gangguan pernapasanyang mengancam jiwa.

Gejala mungkin termasuk diaforesis, splinting dinding

dada untuk meredakan nyeri pleuritik, dan sianosis(dalam kasus tension pneumothorax).

Temuan pada auskultasi paru juga bervariasitergantung pada luasnya pneumotoraks.

Pasien yang terkena juga dapat mengungkapkandiubah perubahan status mental, termasuk penurunankewaspadaan dan / atau kesadaran (sebuah temuanlangka)


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Respiratory findings may include the following: Respiratory distress (considered a universal finding) or respiratory arrest

Tachypnea (or bradypnea as a preterminal event)

Asymmetric lung expansion: A mediastinal and tracheal shift to thecontralateral side can occur with a large tension pneumothorax.

Distant or absent breath sounds: Unilaterally decreased or absent lungsounds is a common finding, but decreased air entry may be absent evenin an advanced state of the disease.

Lung sounds transmitted from the unaffected hemithorax are minimalwith auscultation at the midaxillary line

Hyperresonance on percussion: This is a rare finding and may be absent

even in an advanced state of the disease. Decreased tactile fremitus

Adventitious lung sounds (crackles, wheeze; an ipsilateral finding)


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Cardiovascular findings may include the following: Tachycardia: This is the most common finding. If the heart rate is

faster than 135 beats per minute (bpm), tension pneumothorax islikely.

Pulsus paradoxus

Hypotension: This should be considered as an inconsistentlypresent finding; although hypotension is typically considered a keysign of a tension pneumothorax, studies suggest that hypotensioncan be delayed until its appearance immediately precedescardiovascular collapse.

Jugular venous distention: This is generally seen in tension

pneumothorax, although it may be absent if hypotension is severe. Cardiac apical displacement: This is a rare finding.


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Work up

Arterial Blood Gas Analysis

Chest Radiography

Other Radiographs and Translumination

Contrast-Enhanced Esophagography

Chest CT Scanning


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Medication summary

Local Anesthetics Lidocaine hydrochloride (Xylocaine, LidaMantle, Anestacon)

Opiate Fentanyl citrate (Sublimaze)

Morphine (Astramorph, Infumorph 200, MS Contin, Oramorph SR)

Analgesics Benzodiazepines

Midazolam

Lorazepam (Ativan)

Antibiotics

Doxycycline (Vibramycin, Vibra-Tabs, Doryx) Cefazolin (Kefzol)


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Complications

Hypoxemic respiratory failure Respiratory or cardiac arrest

Hemopneumothorax

Bronchopulmonary fistula

Pulmonary edema (following lung reexpansion)

Empyema

Pneumomediastinum

Pneumopericardium

Pneumoperitoneum

Pyopneumothorax


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Differential Diagnoses

Acute Coronary Syndrome Acute Respiratory Distress Syndrome

Aortic Dissection

Congestive Heart Failure and Pulmonary Edema Esophageal Rupture and Tears

Myocardial Infarction

Pericarditis and Cardiac Tamponade

Pulmonary Embolism Rib Fracture


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Parah dan persisten asma yang tidak

menanggapi terapi konvensional

Suatu bentuk parah asma di mana obstruksi

jalan napas tidak responsif terhadap terapi

obat biasa.

* Status Asthmaticus


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Faktor-faktor pencetus berikut mungkin bertanggung

jawab atas kerusakan akut dalamnegara status dan

harus dievaluasi dan ditangani untuk terapi untuk

menjadi sukses:1. Infection :Viruses, bacteria, fungi (bronchitis,

pneumonia)

2. Allergic Factors :

Pollens, animal danders, dusts, foods,

drugs

Precipitating Factors


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3. Irritative Factors :

Dusts, fumes, smoke (air pollutants)

4. Trigger Mech.Sinobronchitic disease, nasal

polypi, otitis media 5. Emotional :

Stress, fatigue


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genetic predisposition

environmental factors

Patients often have a history of atopy Gastroesophageal reflux disease is another

risk factor for asthma

Risk factors


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Risk factors for asthma also include the following:

Viral infections

Air pollutants - Eg, dust, cigarette smoke, and

industrial pollutants Medications - Including beta-blockers, aspirin,

and nonsteroidal anti-inflammatory drugs(NSAIDs)

Cold temperature

Exercise

M h i f St t A th ti


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Mechanisms of Status Asthmaticus

Mucous

Hypersecretion

Bronchospasm

Mucosal edema

Increased resistance to air flow

Atelectasis Uneven

ventilation

AbnormalV/Q

Hyperinflation

deadspace compliance

alveolar

hypoventilation WOB

pCO2pO2


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Asthma

Lower airway obstruction

Bronchospasm

Edema

Mucus

Caused by

Irritants

Respiratory infection

Emotional distress


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Asthma

Underlying Problem: VENTILATION ANDINFLAMMATION

Assessment/Associated Symptoms

Non productive cough Wheezing

Speech dyspneaone word sentences

Use of accessory muscles

Status Asthmaticusnot responding to treatment


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Classification asthma disease

Intermitten

Mild persistent

Moderate persistent

Hard persistent


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Episodic of Asthma

Mild

Moderate

Hard

Apnoe, emergency


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REFERENCES

Longo D, Fauci AS, Kasper D, Hauser S, Jameson Jl,

Loscalzo J, editors. Harrisons principles of internal

medicine. 18thed. New York: McGraw-Hill, 2011.

Sjaifoellah Noer, Sarwono Waspadji, Muin RachmanA, Lesmana LA, Djoko Widodo, dkk, editor. Ilmu

Penyakit Dalam. Jilid I edisi III. Jakarta: FKUI, 1996.

John, Md. Marx, Robert, Md. Hockberger, editors.

Rosen's Emergency Medicine: Concepts and ClinicalPractice. 7thed. Philadelphia: Mosby Elsevier, 2007.

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