respiratory failure part2

7/27/2019 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

respiratory failure part2

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