Alteration to Respiratory FunctionNURS6012015

Objectives

To understand the pathophysiology of asthma, COPD and pneumonia (LO1)

To understand the concepts of altered perfusion, ventilation, diffusion and hypoxemia (LO1)

To be able to explain the pathophysiological rationale for assessment and interventions (LO2) for patients with altered respiratory function

Concepts

Perfusion Ventilation Diffusion Inflammatory response Hypoxaemia/hypoxia

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V/Q mismatch

Statistics

Respiratory conditions are the leading cause of hospital admissions for children

COPD affects 15% of the population over 45 years and is the 4th leading cause of death.

85% of COPD is caused by tobacco smoking it costs $1200 a day to treat a child with asthma in hospital

Asthma

Is a chronic inflammatory disorder of the airways It is characterised by:

1. Reversible airway obstruction

2. Airway inflammation

3. Increased airway responsiveness

Asthma Inflammatory chemicals are released from mast cells (IgE mediated response) in airways

Histamine Leukotrienes Prostaglandins Bradykinins Serotonin Cytokines and others... http://glencoe.mcgraw-hill.com/sites/0015081981/student_view0/chapter14/ige_mediated__type_1__hypersensitivity__quiz_2_.html

Pathophysiology of asthmaInflammation causes: denudation of airway epithelium collagen deposits beneath the basement membrane localised oedema in smooth bronchiole walls thick mucus bronchospasm airway wall remodelling vascular congestion impaired mucocilary functioning

Localised oedema Bronchospasm

With the release of chemical mediators, the normal respiratory epithelium is denuded and replaced by goblet cells this results in: Increased mucus oedema inflammatory exudate Hyper-responsiveness of the airway. Asthma Clip

Occurs in response to inflammation of the airway

Inflammatory mediators – such as histamine stimulates parasympathetic receptors and bronchial smooth muscle causing bronchoconstriction

Early and late response

Early response is immediate and results in narrowed airway with thick mucus.

Late response- a second mediator response occurs 6-12 hours after exposure to the trigger.

Causes epithelial damage, mucosal oedema, impaired ciliary function thus clearance and prolonged bronchoconstriction.

Airway is remodelled (airway thickened, smooth muscle hypertrophy and increase in goblet cells) over time due to frequent inflammation.

Changes to gas exchange Limited expiratory airflow traps air distal to the bronchoconstriction.

What does this mean for the person with asthma?

Trapped air mixes with inspired air in the alveoli and therefore there is reduced gas exchange across the alveolar-capillary membrane

Diffuse wheezing – Dyspnoea and tachypnoea Cough and increased sputum production Chest feels tight Prolonged expiration Tachycardia –early sign of hypoxaemia Decreased PEFR- Pulsus paradoxis- drop in systolic pressure during

inspiration>10mmHg Cyanotic, agitated, restless, exhausted and confused-asthma is

regarded as severe and life-threatening.

Asthma Symptoms

Hypoxaemia

Is deficient blood oxygen as measured by low arterial O2 and low Hb saturation

(Copstead and Banasik (2010, p. 529)

When the Pa02 <60mmHg the patient is hypoxaemic

Central chemoreceptors in the medullary centre respond to changes in ???

Can only be measured accurately by arterial blood gases (ABGs)- taken when clinically indicated and O2 saturations are less than 92%

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Nursing Care: Assessment Health history- Respiratory Cardiac Monitor skin colour and temperature Monitor hydration Monitor LOC Diagnostic tests: PEFR, ABGs, CXR

Respiratory AssessmentINSPECTION INSPECTION AND HEALTH HISTORY

Rate: rapid, normal or slow

Depth:

Ease: Dyspnoea, orthopnoea, apnoea,

Laboured breathing: continuous or intermittent, becoming worse sudden onset at rest or on exertion (SOBOE)

Rhythm: Is there a variation in the rate of depth of respirations?

Evidence of infection

Cough

Wheeze

Cyanosis

Chest Pain

Sputum

Bad breath

Wheeze noises

Wheezes and other sounds

Nursing interventions and rationale: asthma

Monitor: skin colour, temp and LOC (Cyanosis, cool, clammy skin and changes in LOC indicate worsening hypoxia)

Monitor: respiratory rate and effort, SP02. Tachypnoea, tachycardia and elevated BP are all signs of compromised respiratory status.

Monitor: Peak Expiratory Flow Rate: maximum flow of air achievable from a forced expiration. Recognise changes, patient needs to have previous PEFR.

Nursing interventions and rationale: for the person with asthma

Administer: prescribed medications such as:- salbutamol and a steroid, oxygen to reduce hypoxaemia

Sit up in high-Fowlers- (reduces work of breathing and increases lung expansion especially of the lung bases.)

Increase fluid intake:- to reduce viscosity of secretions-therefore it is easier for the patient to clear these secretions- decrease risk of mucus plugs.

MedicationsType Medications Route

Beta -2 agonistsBronchodilatorReliever

E.g. Salbutamol= Ventolin

?

Anti-cholinergics Atrovent =Ipratropium bromide

InhalerNebuliser

CorticosteroidsSteroidPreventer

Flixitide =Fluticasone

InhalerOralIntravenous

Chronic Obstructive Pulmonary Disease (COPD)

http://www.livingwellwithcopd.com/en/what-is-copd.html

Bronchitis

“Hyper-secretion of mucus and chronic productive cough for at least three months for at least two consecutive years”

http://copd.about.com/od/complicationsofcopd/ig/Complications-Image-Gallery/17099.htm

Emphysema “Abnormal permanent enlargement of the airways and destruction of the alveolar walls”

(Craft, Gordon, & Tiziani, 2011. p 736)

Airflow limitation is caused by changes in lung tissue rather than obstruction.

Develops over a long period of time

Emphysema Normally bacteria or foreign bodies are removed by phagocytosis, however the phagocytes cannot

digest smoke particles and you get protease, collagenase and elastase all digestive enzymes that are now in the alveoli

Loss of elasticity in alveoli and permanent enlargement of airspaces

Alveolar destruction causes large air spaces that are ineffective for gas exchange.

Causes a significant loss of respiratory membrane for gas exchange and a ventilation/perfusion mismatch and hypoxaemia

Air trapped in distal alveoli

Nursing interventions for COPD Medications as prescribed Encourage fluids Place in high-Fowlers Assist with coughing and deep breathing Teach how to use MDIs Reassurance Mouth care Monitor and record nutritional intake-high protein and high energy Skin care – extended use of steroids Promote rest

Possible conflict: what will happen if

the patient still smokes?

Pathophysiology of Pneumonia Pneumococcal pneumonia is most common

cause

Four stages:

Congestion

Red hepatisation

Grey hepatisation

Resolution Retrieved from http://faculty.stcc.edu/AandP/AP/AP2pages/Units21to23/respiration/alveolar.htm

Simons story

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Pathophysiology of Pneumonia RED HEPATISATION: There is massive dilation of the capillaries and the

alveoli are filled with organisms, neutrophils, red blood cells and fibrin. Inflammatory cells invade the alveolar septa.

GREY HEPATISATION: Blood flow decreases and leucocytes and fibrin consolidate in the affected part of the lung.

RESOLUTION: macrophages ingest and remove neutrophils, fibrin and bacteria.

PneumoniaSIGNS AND SYMPTOMS ASSESSMENT FINDINGS

Temperature

Chills, cough and purulent sputum

Crackles

Pain

Hypoxaemic

Tachypnoea and dyspnoea

Dehydrated

Productive cough

Definitive diagnosis needs an x-ray

Change in rate, rhythm, ease of breathing.

Asymmetrical chest movements.

Nasal flaring

Accessory muscles use.

Crackles on auscultation.

Dullness on percussion.

Pink, rusty, purulent, green, yellow or white sputum.

Pain.

Nursing interventions and rationale: pneumonia.

Monitor and document : Administer Position: Increase Educate:

Homework What is the rationale behind your interventions for the patient with pneumonia?

Is the pathophysiological rationale the same? How is it different?

Where do you find the rationale?

Summary Learning Outcome One- pathophysiology of asthma, COPD and pneumonia

Learning Outcome Two: respiratory assessment and interventions- cares and medications- why are you doing this assessment or interventions for this patient what are you expecting to find?

Linking the two together are concepts –perfusion, ventilation, diffusion and

hypoxaemia .

References Copstead-Kirkhorn, L-E. C., & Banasik, J. L. (Eds.). (2010). Pathophysiology (4th ed.). St Louis, Missouri: Elsevier

Saunders.

Craft, J. Gordon, C. & Tiziani, A. (2011). Understanding pathophysiology. Victoria, Australia:Elsevier.

Marieb, E. N., & Hoehn, K. (2007). Human anatomy & physiology (6th ed.). Sydney: Pearson Benjamin Cummings

McCance, K.L. and Heuther, S.E (2010). Pathophysiology The Biologic Basis for Disease in Adults and Children (6th Ed.). Philadelphia: Mosby Elsevier

McGraw –Hill Retrieved from: http://glencoe.mcgraw-hill.com/sites/0015081981/

Nucleus Medical Media (2009). Acute Respiratory Distress Syndrome (ARDS). Smart Imagebase. Retrieved Apr 1, 2012, from http://ebsco.smartimagebase.com/acute-respiratory-distress-syndrome-ards/view-item?ItemID=7763

http://www.asthmafoundation.org.nz/files/PDF-files/AsthmaSelfManagementPlan08_final.pdf

http://www.nhs.uk/Conditions/Chronic-obstructive-pulmonary-disease/Pages/Lynnsstory.aspx