Download Respiratory End of Phase

Respiratory End of Phase
Joseph Dugan and Brendan Haughey
Things I picked up…
• Focus on core topics (commons common)
• Start to apply knowledge in clinical scenarios
• Link anatomy-physiology-micro-clinical skills
• Asthma
Acid-Base Balance (ABG)
• COPD
PFT’s
• LRTI/Pneumonia Clinical scenarios
Airway – the basics
3 MAIN FUNCTIONS1. Passage of Gas/Gaseous
Exchange
1. Protection of the Lungs
2. Warming/Humidifying air
Respiratory Physiology-BASIC
 Ventilation: Movement of air into and out of lungs
 Compliance: Ease with which lungs can be inflated i.e ↓ in Fibrosis
 Airflow = Pressure Gradient / Airways resistance
-resistance is usually low … except in *Obstruction=ASTHMA/COPD*
 Pressure gradient created by
- Elastic tissue = recoil causing collapse
-Surface tension = created by fluid lining the alveoli
-Negative intrapleural pressure = subatmospheric/draws gas in
 Air is brought in by above gradient which sets up for gaseous
exchange across another gradient
Quick Fact- Surfactant
Surfactant :
– is a natural phospholipid protein
- is produced by TYPE II PNEUMOCTYES
-it decreases the SURFACE TENSION of the lung thus requiring less
NEGATIVE INTRAPLEURAL PRESSURE to keep the lung inflated thus
INCREASING COMPLIANCE
-given to premature neonates to prevent Infant Respiratory Distress
Syndrome
-Common EOP/Physiology Question
Mechanism of Breathing
Lung compliance = ease with which the lungs can be inflated… What diseases DECREASE
compliance?
INSPIRATION = ACTIVE PROCESS
•
Thoracic volume increased by DIAPHRAGM contracting and pulling down creating a gradient
for inflow or air
What innervates the diaphragm? C3,4 and 5 KEEP THE DIAPHRAGM ALIVE
Also EXTERNAL INTERCOSTAL muscles contract increasing width of the thorax
Other ACCESORY MUSCLES (Sternocleidomastoid muscle/Scalenus) are used in quicker inspiration
i.e Asthma Attack /Strenous Exercise
EXPIRATION = MOSTLY PASSIVE
•
‘Quiet expiration’ relies on elastic recoil as the above muscles relax ,HOWEVER this can be
aided by the contraction the ABDOMINAL MUSCLES
Gaseous Exchange 1
Alveolar
membrane is
the gas
exchange
surface
BLOOD-GAS
barrier
DEOXYGENATED Blood arrives from the heart via the pulmonary artery
OXYGENATION occurs across the blood gas barrier and CARBON DIOXIDE
is offloaded, this process is driven by partial pressure gradients (PaO2:PaCO2)
Gaseous Exchange 2
• Efficiency of gas exchange in lungs is often
measured in terms of the TRANSFER FACTOR
for carbon monoxide
Transfer Factor =Rate of CO absorption /
Alveolar PaCO
Oxygen Dissociation Curve
“Haemoglobins affinity for oxygen” - this is, how readily
haemoglobin acquires and releases oxygen molecules into the
fluid that surrounds it… This is VARIABLE…
…………………………….
THE OXYGEN DISSCIATION CURVE
Each Haemoglobin molecule can potentially bind FOUR O2
molecules, as this number increases the affinity increases
Factors Affecting the Curve
(Bohr Shift – right Shift)
This represents the need for higher oxygen
levels to saturate haemoglobin – however, it
therefore allows easier extraction of Oxygen
from haemoglobin by the tissues that need
it
THINGS THAT MOVE CURVE RIGHT:
1. CO2 Conc. increase
2. Increase Temperature
3. Increase in 2,3-DPG Levels
4. Decrease in pH
ABG’s and Acid-Base Balance
Acid-Base Balance
• Common EOP question – ABG analysis
pH
7.35-7.45
Pa02
>10kPA
PaCO2
3.5-6 kPA
HCO3
22-30 mmol/L
Base Excess
+ 2 to - 2
N.B- These values will vary in different resources- normal values
will always be given in the exam
Back to chemistry…. Henderson-Hasselbach
CO2 = ACIDIC
HCO3= BASIC
Reaction is catalysed by CARBONIC ANHYDRASE (H2CO3)
Interpretation Acid-Base Quick guide
1. pH = is the patient Acidotic or Alkalotic
• Acidosis can either be from too much CO2 (Respiratory) or not
enough HCO3 (Metabolic)
• AlkalosisIs usually the result of too little acid (loss of H+) or too little
CO2 (Not common)
2. CO2=
is the CO2 high or low?
• High CO2 – This is indicative of Respiratory acidosis – the
retention of CO2
• Low/Normal – Look at theHCO3 / Consider Hyperventilation
3.HCO3= is the HCO3 high or low?
• Low HCO3 without high CO2 = Metabolic acidosis
Condition
Gas Changes
Underlying Cause
Respiratory Acidosis
↑PaCO2
Respiratory Failure/COPD
Respiratory Alkalosis
↓PaCO2 + HIGH Pa02
Hyperventilation
Metabolic Acidosis
↓HCO3
DKA,Renal Failure, Lactic
Acidosis, Acid Ingestion
Metabolic Alkalosis
↑HCO3
Acid loss –
vomiting/diarrhoea
Usually on the End of Phase paper there is a case of acidosis – you must be able to
tell the difference between a metabolic and respiratory acidosis i.e High CO2 or Low
HCO3 respectively (then consider compensation)
IF IN DOUBT GO BACK TO BASIC CHEM – CO2 ACIDIC / HCO3 BASIC
Respiratory Failure
• Two types
TYPE I = Hypoxia in isolation
TYPE II= Hypoxia plus Hypercapnia ( CO2 retention)
• Clinical significance – The drive to breath comes from
CO2 levels in the body, however patients with
longstanding COPD can loose this stimulation as they
chronically retain CO2- thus they rely on a HYPOXIC
DRIVE to maintain respiration
• Thus delivering these ‘Type 2’ patients with high levels
of O2 can reduce the drive to breath thus reducing
respiratory rate = NOT GOOD
• This is overcome by maintaning a lower target
saturation and using special oxygen deliver devices like
Venturi Masks
Respiratory Infections- Pneumonia
LRTI – Lower Respiratory Tract infection
Signs and Symptoms= SOB/ Fever/ Productive Cough/ Confusion/ Chest pain
On Examination= Coarse crepitations in lung fields / Decreased Saturations / Pyrexia
Investigations = WCC raised/ CRP raised/ CXR shows consolidation/ Sputum or Blood Culture +ve/
Urinary antigen for Legionella
Two main types – CAP = Community Acquired
- HAP= Hospital Acquired > 2 days after admission
Causative Organisms CAP
1.Viral
2. Strep Pneumoniae
3.Humophilus Influenza
4.Staph Aureus
Atypical Organisms = Mycoplasma Pneumonia and Legionella Pneumophillia
Degree of severity of CAP quantified using CURB 65 score (don’t
think you need to know in detail)
At risk groups = Extremes of age
Immunosupressed (Iatrogenic/HIV etc)
CF/COPD/Asthmatics
First Line Treatment = Amoxicillin +/- Clarithromycin
Or if Penicillin alergic Doxycycline
Severe = Co-Amoxiclav IV + Clarithromycin IV
Pulmonary Function Tests
• Spirometry
– FEV1
– FVC
• Peak Flow
Spirometry
Describe precisely what FEV1 and FVC
• FEV1 Forced expired volume in one second after full inspiration
• FVC (forced vital capacity) total forced expiratory volume after full inspiration
Spirometry indicates the presence of an
abnormality if any of the following are recorded:
• FEV1 < 80% predicted
• FVC < 80% predicted
• FEV1/FVC ratio <0.7
Obstructive disorder:
• FEV1 reduced
• FVC is usually reduced but to a lesser extent
than FEV1
• FEV1/FVC ratio reduced (<0.7)
Restrictive disorder:
• FEV1 reduced
• FVC reduced
• FEV1/FVC ratio normal (>0.7)
Asthma
Reversible airway obstruction.
SOB, cough, wheeze.
• Narrowing of large and small airways
due to immune hyper-reactivity.
• Bronchial smooth muscle contraction.
• Inflammation in the airway wall with a
cellular infiltrate including eosinophils,
mediator release and wall oedema
• Increased mucus production.
• Spirometry: FEV1 would be markedly
reduced. FVC would be reduced to a
lesser extent. FEV1 / FVC ratio <0.7
• Obstructive defect, typically seen in
asthma
Medications in Asthma
• B2 Agonists - Salbutamol
• Acts on G-protein coupled
receptors (beta 2 receptors)
leading to their activation and
increasing cAMP in airway smooth
muscle to produce
bronchodilation.
• Side effects include tremor,
tachycardia, hypokalaemia.
• Inhaled corticosteroid (Budesonide)
• Cause repression (decreased
transcription) of proteins mediating
inflammation, or activation (increased
transcription) of proteins that suppress
inflammation.
• Steroid side effects involve alteration of
protein (skin thinning ,osteoporosis,
muscle wasting) carbohydrate( glucose
intolerance, diabetes) and fat (buffalo
hump, central obesity) metabolism.
– Inhaled - candida
COPD
• Chronic inflammatory
condition causing progressive
airflow obstruction secondary
to parenchymal disease
• Symptoms – SOB, cough,
sputum, wheeze
• Causes – Smoking, Alpha 1antitrypsen deficiency
(emphysema and cirrhosis)
• FEV1/FVC <0.7 – obstructive
• Non-reversible cf. asthma
Treatment
• Similar to asthma (inhaled b2
agonist/antimuscarinics)
• Stop smoking!
Anatomy
• Using a diagram describe the gross anatomy of the lungs including their
vascular connections to the heart.
• Know the mechanism of breathing – Skeletal and Muscular Anatomy
• What accessory muscles of breathing do you know?
• Know the cross section of roots and hilia of the lungs.
• Which lung has three lobes and which has two lobes? What are the lobes
named?
• What are the names of the fissures in each lung?
• What side of the bronchial tree do foreign bodies normally lodge in and
why?
• What is the narrowest point of the upper airway?
Right Lung
Left Lung
References
• https://www.brit-thoracic.org.uk/documentlibrary/delivery-of-respiratorycare/spirometry/spirometry-in-practice/