Respiratory Failure Part2
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Definition Respiratory failure is said to exist when the lung
cannot fulfill its primary function of adequate gas
exchange. Essentially this means a fall in PaO2 with or
without a rise in PaCO2.
In practice
PaO2 less than 8kpa(60mmHg)while breathing roomair
Or a PaCO2 greater than 6.5kpa(49mmHg)
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ClassificationAccording to Duration Acute occurring over minutes or hours
Chronic occurring over days or months
Pathophysiology Hypoxaemic respiratory failure (Type 1) Characterized
by a PaO2 of less than 60mmHg with a normal or lowPaCO2(< or = to 40mmHg)
Hypercapnic respiratory failure (Type11) Characterizedby a PaCO2 of more than 49mmHg. Also Hypoxaemia
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Respiration Respiration involves 3 processes
Transfer of O2 across the alveolus
Transport of O2 to the tissues Removal of carbon dioxide from the alveolus and then
into the environment.
Respiratory failure can arise from the abnormality of
any components Airways, alveoli, CNS, peripheral nervous system,
respiratory muscles and chest wall
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PhysiologyRespiration occurs at the alveolar capillary units of the
lung
Exchange of O2 and CO2 b/w alveolar gas and blood takes
place.
Each molecule of HB combines with a maximum of1.36ml of oxygen level depends on PaO2.
O2 dissociation curve sigmoid in shape.
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Oxygen dissociation curve
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Physiology The CO2 is transported in 3 ways
In simple solution carbonic acid
As bicarbonate Combined with HB as carbamino compd
In steady state
CO2 production equals CO2 elimination
PaCO2=K(VCO2/VA) VA (Alveolar ventilation) VCO2 isCO2 production
K is a constant (0.863).
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VE=VA+ VD VA= VE- VD
Hypercapnia occurs with
Decreased minute ventilation or Increased dead space
Usually only slight A to a PaO2 diff. An increase above 15-20mmHg indicates pulmonary disease
In Ideal Gas exchange
Ventilation and perfusion are matched High V/Q Low V/Q
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Pathophysiologic causes of Acute RFHypoventilation
V/Q mismatch
Shunt
Diffusionabnormality
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PathophysiologyAcute respiratory failure
Hypoventilation Type 11 Resp. Failure
Occurs when ventilation is
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PathophysiologyV/Q mismatch most common cause of Type 1
Hypoxaemic Respiratory failure
Low V/Q ratio may occur Decrease in ventilation secondary to
Airway or interstitial disease
Overperfusion in the presence of normal ventilation
Pulmonary embolism 100% oxygen very effective
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Diffusion deficit
Less common
Due to abnormality of alveolar membrane
Decrease in number of alveoli
Cardiogenic and non cardiogenic pulmonary oedema
Fibrotic lung disease
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Pathophysiology Shunt
Admixture of oxygenated and deoxygenated blood
Hypoxia persistent with 100% oxygen# Hypercapnia when shunt >60%
Disease processes
Intrapulmonary, intracardiac, Pneumonia atelactasiscollapse, haemorrhage, cardiogenic and non cardiogenicpulmonary oedema A/V malformation
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AetiologyAetiology
Affecting the brain Depression of neural drive Drugs narcotics poisons trauma tumors infection myxoedema,
Affecting the nerves and muscles Guillain Barre Myasthenia Gravis Poliomyelitis Muscular
dystrophy
Affecting upper airways Tumours oedema foreign body trauma
Affecting the chest wall Crushed chest, Kyphoscoliosis, morbid obesity
Affecting the lower airways and lung parenchyma COPD, ARDS, Trauma, infection neoplasm
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Causes Type 1
Associated with conditions affecting the interstitiumalveolar wall Acute causes
Severe Asthma, cardiogenic and non cardiogenic pulmonaryoedema pulmonary embolus ARDS Pneumonia
Chronic causes
COPD, Lymphangitis carcinomatosis fibrosing alveolitispneumoconiosis
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Type 11
Associated with alveolar hypoventilation Acute causes
Drug overdose with hypnotics opiates narcotics tranquilizerspoisoning Myasthenia gravis Guillain Barre syndromeCrushed chest poliomyelitis
Chronic causes
COPD Primary alveolar hypoventilation Kyphoscoliosis
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Clinical Features This reflects the underlying disease condition
examples such as pneumonia, asthma, pulmonaryoedema COPD are readily apparent
Also symptoms and signs of Hypoxia with or withoutHypercapnia
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Hypoxia Cyanosis easy to detect in polycythaemia diff in
anaemia
Restlessness agitation irritability clouding ofconsciousness convulsions tachypnoea tachycardiacoma death. Cardiac arrhythmias
Pulmonary hypertension with or without cor
pulmonale Polycythaemia
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CYANOSIS
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Hypercapnia Dyspnoea
Dilatation of cerebral blood vessels with increasesintracranial pressure cerebral oedema papilloedemaheadache
Flapping tremor (asterexis) stupor Coma
Hypoxaemia hypercapnia acidosis cause
Increased gastric acid production In severe cases gastric dilatation and paralytic ileus.
Haemorrhage stress ulcers
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Acute respiratory failure
life-threatening derangements in arterial blood gasesand acid-base status PH low less than 7.3
Chronic respiratory failure
Symptoms less dramatic
Usually PH only slightly decreased due to renal
compensation Polycythaemia
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InvestigationsArterial blood gases
FBC Anemia, polycythaemia
Chemistry- EUC K Mg Ph cardiac enzymesCXR
ECG- arrhythmias may show CVS cause
Echocardiography Rt heart catheterization
Lung Function tests
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Distinction between Noncardiogenic (ARDS) and
Cardiogenic pulmonary edema
ARDSPulmonary edema
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Diagnosis Depends on demonstration of abnormal Blood Gas
tensions
Laboratory diagnosis
Clinical features may be non specific and verysignificant respiratory failure may be present withoutdramatic symptoms
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Management Priorities depend on aetiology.
Generally
Admit intensive care unit Maintain adequate airwayVital
Correction of Hypoxaemia mostimportant
Threat to organ function
Address Hypercapnia and respiratory acidosis Ventilator management
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Type 1 Treatment with Oxygen using nasal cannulae oxygen
masks
Treatment of underlying cause
Asthma
Pneumonia
Antibiotics
Pulmonary embolism If hypoxaemia persists assisted ventilation
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Type11 Commonest cause is COPD Patent airways- remove secretions Phsio
pharyngeal suction
Hypoxaemia Controlled O2 therapy BronchodilatationAntibiotics Diuretics Respiratory stimulantsIf above efforts fail to improve respiratory function
consider assisted ventilation.
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Rx for other causes of type two Respiratory depression sec to drugs give antagonists or
enhance drug removal by dialysis
Myasthenia gravis treated with specific drugs
Guillian Barre respiratory support required forduration of disorder
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Case 1 A 36 yo man who has had a recent viral illness now is
admitted to the ICU with rapidly progressive ascendingparalysis (diagnosed as Guillain-Barre Syndrome). He is
breathing shallowly at 36/min and complains of shortnessof breath. His lungs are clear on exam. CXR shows smalllung volumes without infiltrates. With the patientbreathing room air, ABG are obtained.
pH 7.18PaCO2 68 mm Hg
PaO2 49 mm Hg
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Why is he hypoxemic?A-a O2 gradient
PAO2 = FIO2 PaCO2/0.8
PAO2 = 150 68/0.8 = 150 85= 65
A-aO2 gradient = PAO2 PaO2
= 65 49 = 16
His A-aO2 gradient is minimally increased, although
his PaO2 is significantly reduced.His hypoxemia is due to alveolar hypoventilation.
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Case 2A 65 yo man has smoked cigarettes for 50 yrs. He
has chronic cough with sputum production andchronic dyspnea on exertion (stops once when
climbing 1 flight of stairs). He is now admittedwith several days of increased cough productive ofgreen sputum and is short of breath even at rest.On exam his breathing is labored (32/min) and his
breath sounds are quite distant. The expiratoryphase is greatly prolonged and there are soft
wheezes in expiration.
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Case 2
ABG analysispH=7.38
PCO2=48
PO2=48
O2 sat=78%
How would you describe his ABG?
He is hypoxemic with a respiratory acidosis.
What is the likely mechanism of hypoxemia? Is his hypercarbia acute or chronic?
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Why is he hypoxemic?What is his A-a O2 gradient?PAO2 = (149-48/0.8) = 149-60 = 89
A-a O2 gradient = 90 48 = 41
His hypoxemia is predominantly due to V/Q mismatch.
An enormous number of conditions cause hypoxemiadue to V/Q mismatch
disorders effecting pulmonary vascular, airways, oralveolar space
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Mechanical Ventilation Increase PaO2
Lower PaCO2.
Also rests Respiratory muscles
Controlled
Patient assisted
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Mechanical ventilation Negative pressure vs positive pressure
Pressure targeted or volume targeted
8-10L/kg at 10-12 breaths per min Flow triggered or pressure triggered
Use lowest F1O2 that produces SAO2>90%
Or PO2>60mmHg to avoid O2 toxicity
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Negative pressure ventilation
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Assisted Ventilation Non invasive
IPPV PSV CPAP has been used in COPD
Use face mask or nasal mask
Invasive with ETT/ tracheostomy
The most common indication for endotrachealintubation (ETT) is respiratory failure
Several methods PSV IMV SIMV HFPPV Patient monitored closely
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Weaning Patients have to be weaned off ventilator
Should be stable and considerably improved
Depends on length of time on ventilator PaO2 >= to 65mmHg
Techniques
SIMV CPAP PSV
Allow Pt to breath spontaneously for small intervalsgradually increasing the length of time and reducinglength of spontaneous respiration
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DangersWrong position of tube
Obstruction
Mucosal oedema Pneumothorax Barotrauma
Haemothorax
Infection VAP
Ventilator dependence
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Other Modes of Management Extracorporeal gas exchange
Extracorporeal membrane exchange
Extracorporeal carbon dioxide removal
Lung transplantation
Employed in patients with end stage respiratory disease
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Prevention Influenzae and Pneumococcal vaccines
Smoking cessation
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MortalityVaries according to aetiology usually high
30% in COPD
40% in ARDSWorse in Patients with Type11
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http://en.wikipedia.org/wiki/File:Clark1974.jpg -
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FIO2
Ventilationwithout
perfusion(deadspaceventilation)Diffusionabnormali
ty
Perfusion
without
ventilati
Hypoventilati
on
Normal
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ARDSAlso called non cardiogenic pulmonary oedema
Adult respiratory distress syndrome
Increased permeability pulmonary oedema Often accompanied by MODS MOF
Renal
Hepatic
cardiac
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CAUSESSepsis, pneumonia Trauma Multiplefractures,pulmonarycontusion
Aspiration, Near drowning, toxic inhalationAcute Pancreatitis
Multiple Blood transfusions
Drug toxicity, methadone overdose
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ARDS
Insult direct or indirect
Activation of inflammatory cells
Damage to alveolar capillary membrane
Increased permeability
Influx of protein rich exudate and inflammatory cells dysfunction ofsurfactant
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Pathophysiology DAD Lung capillary endothelial damage
Early phase exudative
Secondary stage fibroproliferative Two types of Alveolar cells
Type 1 easily injured 99%
Type 11 resistant
Surfactant production Differentiates into type1 Alveolar collapse defect in repair
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Neutrophils
Cytokines
Leukotrienes TNF
Macrophage Inhibitory factor
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Clinical featuresAcute onset
Tachypnoea Dyspnoea
Wide spread Crepitations some rhonchi Refractory hypoxaemia
Bilateral infiltrates in the lung fields
Normal pulmonary capillary wedge pressure
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ARDS
PaO2/FiO2 < 200
ALI
PaO2/FiO2
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Management Treatment of underlying cause oxygen
Anti inflammatory Steroids
Vasodilators Nitric Acid
Surfactant
Prone position
Antibiotics for sepsis
Diuretics fluid restriction
Assisted ventilation