Showing posts with label Pulmunology. Show all posts
Showing posts with label Pulmunology. Show all posts

Thursday, April 30, 2020

BPAP - Bilevel Positive Airway Pressure Ventilation

Bilevel noninvasive ventilation provides:
1) IPAP - inspiratory positive airway pressure and
2) EPAP - expiratory PAP at two different levels.

This is typically delivered with a tight fitting nasal or face mask which allows for the development of positive airway pressure.
The noninvasive therapy should be initiated as early as possible in case of respiratory failure and is best used for short term.

"Delta PAP" is the difference between IPAP and EPAP. It directly correlates with the tidal volume delivered. If the "delta PAP" is larger then the tidal volume will be larger and hence it will provide a better alveolar ventilation.

It is quite safe to start the following initial settings:

1) EPAP 3 to 5 cm H2O (2 - 4 mm Hg) – It can be increased to around 10 cm H2O if ever the oxygenation remains inadequate tidal volume.

2) IPAP 8 to 12 cm H2O (6 - 9 mm Hg) – This can be increased in increments of 2 cm H2O as tolerated by the patient, to a maximum of 20 cm H2O. Up titration will depend on the degree of dyspnea, respiratory rate and patient-ventilator synchrony.

3) Bilevel NIV (BPAP) mode - The spontaneous/timed (S/T) setting with a backup rate of 8 to 12 breaths/minute is the preferred mode since it ensures that all breaths are supported and that a minimum respiratory rate is provided if the patient hypoventilates.

Saturday, January 2, 2016


Reading chest radiograph - Penetration


Penetration is one of the five technical factors that help you in determining whether a radiograph is technically adequate.


If a frontal chest radiograph is adequately penetrated, you should be able to see the thoracic spine through the heart shadow.

In the radiograph above, we can see the thoracic spine through the heart shadow (solid white line).

It means that the penetration is inadequate. The radiograph will appear as too white. We will not be able to see the thoracic spine through the heart. This can lead us into making interpretation errors.
1) The pulmonary markings may appear more prominent and these can be mistaken for being due to a congestive heart failure or pulmonary fibrosis.
2) The left lung base will appear opaque thus obscuring the left hemidiaphragm. This can mimic or hide a true disease in the left lower lung field e.g. left lower lobe pneumonia or left pleural effusion.

To avoid these misinterpretations always correlate clinically. Also if you are suspecting a congestive heart failure, look for other signs apart from increased pulmonary markings e.g. effusions, Kerley lines etc. A lateral radiograph will also help us when faced with these dilemmas.

In this frontal chest radiograph we can see that there is under penetration.

The solid black line shows that the thoracic spine cannot be seen through the heart shadow.

The broken black lines show that the left hemidiaphragm is not clearly visible.

In this case, the lung markings will appear decreased or absent. The patient may be mistaken of having a pneumothorax or emphysema. We may also miss a pulmonary nodule if the radiograph is too dark.

This is an example of an over penetrated chest radiograph.

At first glance we may suspect emphysema in this patient because of the increased lucency at the apices but when we look at the diaphragm we find that it is not flattened, which means there is no hyperinflation as expected for a case of emphysema.

First published on: 01 January 2016

Monday, January 19, 2015


COPD exacerbation - definition, assessment, management

COPD exacerbation:

Exacerbation of COPD is defined as an acute episode, characterized by the worsening of the patient’s respiratory symptoms that is beyond normal daily variations and that will eventually lead to a change in his medications.
Those having 2 or more exacerbations per year are known as “frequent exacerbators”.

Precipitating factors:
1) Respiratory tract infections – viral or bacterial. Most common cause. There may be an increased bacterial burden in the lower airways or new strains of bacteria are acquired during an exacerbation. Commonly implicated viruses
include rhinovirus, respiratory syncytial virus, coronavirus and influenza virus.
2) Air pollution.
3) Interruption of maintenance therapy.
4) Unknown causes – 30% cases.

Diagnosis should be made clinically whereby the patient complains of an acute aggravation of his symptoms out of proportion to his day to day variations. 

Medical history:
1) Severity of COPD before this exacerbation
2) Duration of the worsening or any new symptoms
3) Number of previous exacerbations or hospitalizations
4) Associated comorbidities
5) Present medications
6) Previous uses of mechanical ventilation.
Clinical examination:
1) Use of accessory respiratory muscles or paradoxical chest wall movements
2) Development of central cyanosis or exacerbation of pre-existing cyanosis
3) Change in mental status
4) Development of peripheral edema
5) Hemodynamic instability

Tests to assess severity include:
1) Pulse oximetry – good for monitoring.
2) Arterial blood gases and acid base status – shows whether there is an acute or acute on chronic respiratory failure.
3) Chest radiography – excludes alternative diagnoses and can show infections.
4) EKG – may help to assess any pre-existing cardiac problems.
5) Complete blood count – white cells may be elevated, hematocrit may be elevated
6) Blood biochemistry.
Spirometry is difficult to perform during an exacerbation and it may not be of enough accuracy. Therefore it is not recommended.

More than 80% of cases can be managed as outpatients but if the following conditions are seen, it is better to admit and if necessary give intensive care:
1) Dyspnea occurring at rest
2) Old age
3) Frequent exacerbator
4) Failure of response to change in/addition of medication to control the exacerbation
5) New onset of arrhythmias or peripheral edema.

Medical therapy consists of:
1) Short acting inhaled bronchodilators – beta-2 agonists with or without anti-cholinergics are preferred. It is better to use a nebulizer as the patient usually is dyspneic and lacks coordination to inhale from a metered-dose inhaler. IV methylxanthines are considered as second line of therapy for bronchodilation and are to be used only in selected cases, especially if there is poor response to short acting inhaled bronchodilators.
2) Corticosteroids – oral prednisone 40 mg/day for 5 days has been shown to shorten recovery time and improve lung function as well as arterial hypoxemia.
3) Antibiotics – these are indicated if the patient has clinical signs of bacterial infections e.g. increased in sputum purulence.  Procalcitonin III may help to indicate antibiotic therapy as it is increased in cases of bacterial infections. Usually in the following conditions antibiotics should be considered:
- 3 cardinal symptoms present: increase in dyspnea, sputum volume and sputum purulence,
- 2 cardinal symptoms, with purulence being one of the symptoms,
Antibiotics are recommended for 5-10 days.
4) Adjunct therapies – proper control of comorbidities is advised. Thromboprophylactic measures should be enhanced.

Respiratory support:
1) Oxygen therapy: Oxygen is titrated to correct the hypoxemia of the patient aiming to achieve a saturation of 88-92%. Usually Venturi masks are preferred to nasal prongs. After 30-60 minutes of oxygen therapy, arterial blood gases should be checked.
2) Non-invasive mechanical support
3) Invasive mechanical support.

Sunday, October 6, 2013


Effect of weather on COPD

Exacerbations of COPD are more commonly seen during the winter season (nearly 1.6 times more frequently). The main cause of these exacerbations is infection with the respiratory virus, rhinovirus.
Frequent exacerbations have been shown to lead to a faster decline in the lung function, poorer quality of life and increased mortality.
A recent study showed that COPD exacerbations in colder periods of the year take longer to recover from and are more likely to involve cough or coryzal symptoms. The exacerbations in the cold seasons also have a greater impact on daily activity, with patients spending more time indoors and being more likely to be hospitalized with respiratory viral infection.

Saturday, February 16, 2013


Respiratory failure - Definition, classification and difference between acute and chronic type

Respiratory failure may be classified as hypercapnic or hypoxemic.
Hypercapnic respiratory failure is defined as an arterial PCO2 (PaCO2 ) greater than 45mmHg.
Hypoxemic respiratory failure is defined as an arterial PO2 (PaO2 ) less than 55 mmHg when the fraction of oxygen in inspired air (FiO2) is 0.60 or greater.
In many cases, hypercapnic and hypoxemic respiratory failure coexist.

Distinctions between acute and chronic respiratory failure are summarized in the table below.

In general, acute hypercapnic respiratory failure is defined as a PaCO2 greater than 45 mmHg with accompanying acidemia (pH less than 7.30). The physiological effect of a sudden increase in PaCO2
depends on the prevailing level of serum bicarbonate anion. In patients with chronic hypercapnic respiratory failure e.g. COPD, a long-standing increase in PaCO2 results in renal compensation and an increased serum bicarbonate concentration. A superimposed acute increase in PaCO2 has a less dramatic effect than does a comparable increase in a patient with a normal bicarbonate level.

Distinction between acute and chronic hypoxemic respiratory failure may not be readily made on the basis of arterial blood gas values only. The presence of markers of chronic hypoxemia (e.g., polycythemia or cor pulmonale) provides clues to a long-standing disorder, whereas abrupt changes in mental status suggest an acute event.

Sunday, December 23, 2012

COPD - History and physical findings


The three most common symptoms in COPD are
1) cough,
2) sputum production and
3) exertional dyspnea.

Many patients will have the above named symptoms for months or years. They will seek medical attention only when there will be an episode of acute exacerbation. However, a careful history usually reveals the presence of symptoms prior to the acute exacerbation.

Exertional dyspnea is often described as
1) increased effort to breathe,
2) heaviness,
3) air hunger or
4) gasping.

The dyspnea is more when the patient does activities involving significant arm work, particularly at or above shoulder level. Conversely, activities that allow the patient to brace the arms and use accessory muscles of respiration are better tolerated.e.g. pushing a shopping cart, walking on a treadmill or pushing a wheelchair. As COPD advances, the principal feature is worsening dyspnea on exertion with increasing intrusion on the ability to perform vocational or avocational activities. In the most advanced stages, patients are breathless doing simple activities of daily living.

Physical findings:

In the early stages of COPD, patients usually have an entirely normal physical examination.
Current smokers may have signs of active smoking, including an odour of smoke or nicotine staining of fingernails.
In patients with more severe disease, we may note a prolonged expiratory phase and may include expiratory wheezing. In addition, signs of hyperinflation include a barrel chest and enlarged lung volumes with poor diaphragmatic oscillations as assessed by percussion. Patients may also exhibit use of accessory muscles of respiration, sitting in the characteristic "tripod" position to facilitate the actions of the sternocleidomastoid, scalene and intercostal muscles. Patients may develop cyanosis, visible in the lips and nail beds.

Although traditional teaching is that patients with predominant emphysema, termed "pink puffers," are thin and noncyanotic at rest and have prominent use of accessory muscles, and patients with chronic bronchitis are more likely to be heavy and cyanotic ("blue bloaters"), current evidence demonstrates that most patients have elements of both bronchitis and emphysema and that the physical examination does not reliably differentiate the two entities.

Advanced disease may be accompanied by systemic wasting, with significant weight loss, bitemporal wasting and diffuse loss of subcutaneous adipose tissue. This syndrome has been associated with both inadequate oral intake and elevated levels of inflammatory cytokines. Such wasting is an independent poor prognostic factor in COPD. Some patients with advanced disease have paradoxical inward movement of the rib cage with inspiration (Hoover's sign), the result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation.

Signs of overt right heart failure, termed cor pulmonale, are relatively infrequent since the advent of supplemental oxygen therapy.

Clubbing of the digits is not a sign of COPD and its presence should alert the clinician to initiate an investigation for causes of clubbing. In this population, the development of lung cancer is the most likely explanation for newly developed clubbing.

Friday, November 23, 2012


Barrel shaped chest

Barrel shaped chest is commonly encountered in the clinical setting. It is seen in emphysema, hence also called as emphysematous chest. The anteroposterior diameter is increased (normally transverse:AP diameter is 7:5). The subcostal angle is wide (usually it is acute at around 70 degrees). The angle of Louis is unduly prominent with the sternum more arched. The spine is concave forwards and the ribs are less oblique.

The respiratory movements are diminished bilaterally, with the mediastinum remaining in the central position. On percussion, the lung is hyper-resonant. On auscultation, there is a diminished vesicular breathing with a prolonged expiration. Rhonchi may be present.

Saturday, August 18, 2012


Pulmonary embolism due to metallic mercury

Above is a chest radiograph of a schizophrenic patient. He was delusional about being a doctor. He used to read a lot of medical books and mastered the art of taking blood pressure. During an episode of psychosis, he broke the blood pressure apparatus and injected the mercury into his vein. We can see in the X-ray that there is micro-embolism of the liquid mercury to the pulmonary arterioles, mostly to the dependent areas and the arrow indicates a small pool of the mercury in the right ventricle.

Thursday, July 19, 2012


Chronic Obstructive Pulmonary disease - Definition

COPD is a preventable and treatable systemic disease state characterized by a progressive airflow limitation that is not fully reversible and associated with an abnormal inflammatory response of the lungs to noxious particles and gas.

Note that the new definition according to GOLD/ATS and ERS does not talk anything about the disease being a mixture of chronic bronchitis and emphysema, though these conditions are very frequently encountered in COPD and also the fact of being 'not fully reversible' distinguishes this disease from the other chronic obstructive condition which is bronchial asthma.

Thursday, July 5, 2012

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Centriacinar / Centrilobular emphysema

In a classical lesion, dilated and destroyed respiratory bronchioles coalesce in series and in parallel to produce sharply demarcated emphysematous spaces. They are separated from the acinar periphery (the  lobular septa) by intact alveolar ducts and sacs of normal size, as shown by the diagram below. 

The lesions vary in quality and quantity even within the same lung. There is striking irregularity of involvement of lobules, and even within the same lobule. The lesions are usually more common and become more severe in the upper than in the lower zones of the lung. Most affected are the upper lobe, particularly the posterior and apical segments, and the superior segment of the lower lobe as depicted below. 

This type of emphysema is commonly seen in chronic cigarette smokers. For classification of emphysema, follow this link: Emphysema

Thursday, May 3, 2012


Light's criteria to differentiate between transudates and exudates

The criteria for separating transudates from exudates were published in 1972 by Light and coworkers. They were based on the measurements of serum and pleural fluid protein and LDH. 

The criteria are as follows:

If at least one of the following 3 criteria is present, the fluid is virtually always an exudate and if none is present then the fluid is virtually always a transudate:
1)      Pleural fluid : Serum protein ratio > 0.5
2)      Pleural fluid LDH > 2/3 of the upper limit of the serum reference range
3)      Pleural fluid : Serum LDH ratio > 0.6

An exception to using Light’s criteria is in the setting of CHF treated with diuretics. Normally, in CHF, the effusions are due to an increased capillary hydrostatic pressure and are therefore transudates. But the use of diuretics has been shown to increase the pleural fluid protein and LDH concentrations. Thus we will have a false positive result making the fluid appear as an exudate. It is believed to be due to the action of the diuretic that causes fluid to shift out of the pleural space.

So in cases of diuretic-treated patients having exudative fluid by Light’s criteria, it is recommended to measure the serum : pleural effusion albumin gradient. If the serum albumin minus pleural fluid albumin is > 1.2 g/dL, the patient is likely to have a transudative effusion. Also in cases where one or more of Light’s criteria are met but clinically the patient is thought to have a condition producing a transudative effusion, then we can also measure the protein levels in the serum and pleural fluid. If the difference between these two levels is > 3.1 g/dL, then the fluid is transudative.

If the fluid is transudative, no further investigations are required and the therapy is directed towards the underlying cause of the effusion but if it is transudative then differential cell count, glucose and cytology must at least be sent. 

Thursday, April 26, 2012


Interpretation - Heart borders on Chest X ray

It is at times difficult to interpret a PA chest X-ray as the amount of information present is huge. A systematic approach should always be done. 

One should have the understanding of what is normal. This must include an evaluation of the 
1) soft tissues, 
2) bones and joints, 
3) pleura, lungs, major airways and pulmonary vascularity, 
4) mediastinum and its contents, 
5) heart and its chambers, as well as 
6) the areas seen below the diaphragm and above the thorax.

The heart borders are explained in this post. 
On the right side of the heart the following structures can be identified:
1) Az - Azygous vein
2) A - Ascending aorta
3) S - Superior vena cava
4) RA - Right atrium

On the left side of the heart, we can identify the following:
1) SC - Subclavian artery
2) AA - Aortic arch
3) PA - Pulmonary artery
4) LB - Lower border of pulmonary artery
5) LA - Left atrial appendage
6) LV - Left ventricle

The x-ray on the right side i.e. B shows the actual positioning of the heart in a normal individual. 

Tuesday, October 4, 2011

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Venous thrombo embolism / Pulmonary embolism - Anticoagulation

As soon as a diagnosis of VTE / PE is strongly suspected, anticoagulant therapy should be started unless there are contraindications. Parenteral drugs like unfractionated heparin (standard heparin) and low molecular weight heparin (lovenox) are started and therapy shifted to a long term stable vitamin K antagonist like warfarin.

Unfractionated heparin
The anticoagulant action is by binding to and accelerating the activity of antithrombin III. This inactivates thrombin, factor IXa and Xa and thus prevents further clot formation. The classical regimen for the dosage is a loading dose of 5000 - 10000 units followed by a continuous infusion of 1000 - 1500 units/hour. Unfortunately we all do not have the same weight. So, a more appropriate dosage is a loading dose of 80 units/kg and a continuous infusion of 18 units/kg/hr.

The aim is to achieve a target activated partial thromboplastin time (aPTT) aka partial thromboplastin time with kaolin (PTTK) of 2-3 times the normal laboratory values, the normal values being 30-40 seconds.

The PTTK is checked every 4-6 hours and the infusion is adjusted accordingly.

Low molecular weight heparin
Enoxaparin (lovenox) is given in a dosage of 1 mg/kg twice daily. The advantages over unfractionated heparin is that it binds less to plasma protein and endothelial cells. So the bioavailability is higher and the half life is longer. The dose response is more predictable. No repeated tests are required for monitoring but care must be taken to lower the dosage in patients with renal insufficiency.

This vitamin K antagonist prevents the gamma carboxylation activation of factors II,VII,IX and X, as well as the proteins C and S. The anticoagulant effects appear only after 5 days because factor II has a half life of 5 days.

The dosage to be used initially is between 5 - 10 mg/ day. We should aim for an INR between 2.0 - 3.0.

Warfarin is a difficult drug to dose and monitor as it has multiple drug-drug and drug-food interactions.

Warfarin should be started as soon as the PTTK is within the therapeutic range. The heparin should be continued until a therapeutic INR has overlapped with a therapeutic PTTK for 2 consecutive days. This usually occurs after a minimum of 5 days.

Saturday, September 17, 2011

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Opiods in acute pulmonary edema

The use of I.V morphine in dyspnea from pulmonary edema due to left ventricular failure produces remarkable relief. The proposed mechanisms include: 
1) reduced anxiety ( decreased perception of shortness of breath ), 
2) reduced cardiac preload ( reduced venous tone ) and 
3) decreased cardiac afterload (decreased peripheral resistance ). 

However frusemide remains the treatment of choice. Side effect is respiratory depression at a higher dosage which occurs because of inhibition of the brainstem respiratory mechanism.

Monday, September 12, 2011

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It is caused by an organism known as Bacillus anthracis. The latter is a gram positive, spore-forming rod that is found in soil. The spores can remain viable for years.

Anthrax came to public notice in September 2001 when it was used as a bioweapon delivered through the U.S Postal System causing infection in 22 persons of whom 5 died. In the past i.e. during World War II , anthrax was studied mainly for its potential use as a biological weapon but following the Biological and Toxin Weapons Convention Treaty in 1972, such research was no longer allowed. Still, some nations and extremist groups do work on this agent secretly.

There are 3 major clinical forms of anthrax:
11)      Gastrointestinal anthrax – from ingestion of contaminated meat
22)      Cutaneous  anthrax – from introduction of spores through opening in skin
33)      Inhalational anthrax- inhalation of spores that deposit in the alveolar spaces.

The inhalational form is the one usually used for bioterrorist attack. Once deposited in the alveolar spaces, the macrophages phagocytose them. They are then transported to the mediastinal and peribronchial lymph nodes where they germinate to cause active bacterial growth. The bacteria produce edema toxins and lethal toxin which are later disseminated by blood.

Incubation period: 1-12 days but can go up to 60 days.

Clinical Features:
fever, malaise, chest and abdominal discomfort.

Culture and then microscopy with Gram’s stain. Wright’s stain of peripheral blood film. PCR.
CXR – evolvement from hilar prominence to progressive enlargement of the mediastinum and eventually pleural effusions.

Successful treatment is possible if the condition is diagnosed quickly and antibiotic treatment started promptly.
Ciprofloxacin 500 mg BD for 60 days.
Doxycycline 100mg BD for 60 days.  

Friday, September 2, 2011

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Differences between hemoptysis and hematemesis

1) There is usually a tingling sensation in the throat in hemoptysis while in hematemesis the patient will usually complain from nausea and upset stomach.

2) The blood is usually frothy and bright red in hemoptysis while it is dark red in hematemesis, non-frothy and food particles may also be present at the same time.

3) Blood in hematemesis will give an acidic pH when tested with litmus paper whereas that in hemoptysis will be neutral to alkaline.

4) Stools will be almost always positive for occult blood in hematemesis while it is usually negative in case of hemoptysis. But it can also be positive at times if the patient has swallowed his sputum.

Last reviewed on: 1 September 2015

Thursday, July 14, 2011


Bronchial asthma - Definition of well controlled B.A

Bronchial asthma is considered to be well controlled if the patient experiences cough, shortness of breath and wheezing less than 3 times/week during the day, less than 3 times/month of night time awakenings and no asthma related interference with normal activity.

Recently it has been found that only 1/3rd of asthma patients can be categorized as being into the well controlled group.

Saturday, May 7, 2011


Omalizumab - Anti-IgE Monoclonal Antibodies

It is a new approach to the treatment of asthma. It is a recombinant humanized gamma immunoglobulin (IgG)1 monoclonal antibody that is targeted against the portion of IgE that binds to its receptors (FC -R1 and FC -R2 receptors) on mast cells and other inflammatory cells.

It inhibits the binding of IgE to mast cells but does not activate IgE already bound to these cells and thus does not provoke mast cell degranulation. It may also inhibit IgE synthesis by B lymphocytes.  In addition, omalizumab causes down-regulation of IgE receptors on mast cells and basophils.

Administration of omalizumab to asthmatic individuals for 10 weeks lowers plasma IgE to undetectable levels and significantly reduces the magnitude of both the early and the late bronchospastic responses to antigen challenge. 

Repeated administration lessens asthma severity and reduces the corticosteroid requirement in patients with moderate to severe disease, especially those with a clear environmental antigen precipitating factor, and improves nasal and conjunctival symptoms in patients with perennial or seasonal allergic rhinitis. Omalizumab's most important effect is reduction of the frequency and severity of asthma exacerbations, even while enabling a reduction in corticosteroid requirements.

Omalizumab treatment reduced exacerbations requiring hospitalization by 88%.

Omalizumab is recommended in the guidelines and in a recent review for asthma patients with allergies whose asthma is not controlled with long-acting beta agonist, high-dose inhaled steroids, and leukotriene modifier therapy or when the use of those medications is associated with intolerable side effects.

The patient's pretreatment serum IgE level (IU/mL) and body weight (kg) are used to determine doses (mg) and dosing frequency. Doses of more than 150 mg are divided among more than 1 injection site so that a single injection site never exceeds 150 mg

Thursday, May 5, 2011



Emphysema is defined as an abnormal, permanent dilatation of the airways distal to the terminal bronchioles due to a destruction in the walls.
There are 4 types of emphysema:
1) centriacinar/centrilobular - seen in cigarette smokers
2) panacinar/panlobular - seen in α1-antitrypsin deficiency
3) distal acinar
4) irregular.
Protease- antiprotease imbalance theory as shown in the picture above.

On examination:
Patient will be dyspneic, hyperventilating and have a prolonged expiration. The chest will be barrel shaped.