Respiratory Assessment Case Study with Lung Sounds!!

[gwenith]

I have found what has to be the BEST case study for respiratory assessment!! It even has lung sounds (really really juicy ones too:p)

Trouble is - no answers

So I figure we can all have a go. You don't have to answer every question - you need only have a go at one or two or none and just lurk. You don't have to get 100% - in fact it might be good for the newer people to omit something or have something not quite right so that someone else can pick up on something too. Play devils advocate if you will.

There is no wrong answers just some that will be more right than others.

When enough people have had a turn at answering I will post answers that I have researched and validated.

[gwenith, BSN, RN]

Thanks for responding Angie but yes I was thinking in terms of this from my previous post on signs and symptoms of COPD

(Cor pulmonale) because of the effects chronic hypoxaemia and hypercapnia which include peripheral oedema, raised jugular venous pressure, hepatic congestion,

Not too sure about the acute versus chronic but if you have some info I am ALL ears;)

[UM Review RN, ASN, RN]

This seemed to fit. From the Merck Manual:

http://www.merck.com/mrkshared/mmanual/section16/chapter203/203c.jsp

Acute cor pulmonale usually results from massive pulmonary embolization but often occurs as acute reversible exacerbations of chronic cor pulmonale in patients with COPD, usually during acute respiratory infection. Chronic cor pulmonale is usually caused by COPD (chronic bronchitis, emphysema)

There's more, of course.

[leslie :-D]

This seemed to fit. From the Merck Manual:

http://www.merck.com/mrkshared/mmanual/section16/chapter203/203c.jsp

Acute cor pulmonale usually results from massive pulmonary embolization but often occurs as acute reversible exacerbations of chronic cor pulmonale in patients with COPD, usually during acute respiratory infection. Chronic cor pulmonale is usually caused by COPD (chronic bronchitis, emphysema)

There's more, of course.

i thought cardiac tamponade was the sequelae to cor pulmonale....

[aiki]

the sites are very informative.keep posting!

[gwenith, BSN, RN]

i thought cardiac tamponade was the sequelae to cor pulmonale....

No mate - Cardiac tamponade is where pressure is placed on the myocardium from fluid - usually blood within the pericardium pressing on and restricting the heart.

This is a really really good resourc on Cardiac Tamponade

http://www.cyber-nurse.com/veetac/horrorctam.htm

Thanks Leslie (Earl58) for introducing a new idea into the case study

[gwenith, BSN, RN]

Here are some more resources on Cor pumonale - the first one is the same website as teh Cardiac Tamponade and all I can say is someone has a ripsnorter of a sense of humour:chuckle

http://www.cyber-nurse.com/veetac/horrorcorpul.htm

This site has a good picture

http://health.allrefer.com/health/cor-pulmonale-cor-pulmonale.html

[leslie :-D]

No mate - Cardiac tamponade is where pressure is placed on the myocardium from fluid - usually blood within the pericardium pressing on and restricting the heart.

This is a really really good resourc on Cardiac Tamponade

http://www.cyber-nurse.com/veetac/horrorctam.htm

Thanks Leslie (Earl58) for introducing a new idea into the case study

there's something w/cardiac that stuck w/me in response to acute cor pulmonale....i understand the pathology of the right sided heart failure in cor pulmonale...but if its' acuity deteriorated, it would naturally lead to a cardiopulmonary emergency....is it mediastinal shift i'm thinking of????

oh professor gwenith?????

[jute]

he is developing ARF, what type : Ventilatory

The physical examination indicated that patient had prolonged expiration and wheezes during expiration. These are suggestive of airway obstruction due to the "trapping" of air in the expiratory airway. The decreased pH and elevated blood carbon dioxide confirm acute hypercapnia (elevated carbon dioxide concentrations in the blood) which hasn't yet been compensated for by elevations in circulating bicarbonate concentrations, suggesting a lack of pulmonary function due to acute exacerbation.

[jute]

Treatment includes :- b2-agonist will bind to the adrenergic receptors within the respiratory system. Activation of the adrenergic receptors will stimulate dilation of the airway. Dilation will occur due to the relaxation of the smooth muscle within the walls of the bronchioles. This dilation will decrease the resistance to the flow of air and subsequently increase ventilation.

And corticosteroids if indicated.But antibiotics is the frist line along with b2-agonist.

[jute]

The respiratory muscles are subdivided based on function. The contraction of the inspiratory muscles increases the volume of the thoracic cavity causing the pressure within the alveoli to decrease and air to flow into the alveoli. During quiet (resting) inspiration, the diaphragm, the external intercostals and the parasternal intercostals contract to stimulate inspiration. During forced inspiration the scalenes and the sternocleidomastoid muscles contract to further expand the thoracic cavity. The pectoralis minor muscles also play a minor role in forced inspiration. During quiet breathing, relaxation of these muscles causes the volume of the thoracic cavity to decrease, resulting in expiration. During a forced expiration, the compression of the chest cavity is increased by contraction of the internal intercostal muscles and various abdominal muscles (the external abdominal oblique, internal abdominal oblique, tranversus abdominis and rectus abdominis muscles).