Session 12 Flashcards
Respiratory acidosis
Respiratory acidosis – • When breathing is inadequate (reduced respiratory rate and/or depth) • Inadequate ventilation • Carbon dioxide removal insufficient • CO2 retention
↑CO2 + H2O H2CO3 HCO3- + ↑ H+
• Equation moves to the right • Leads to an increase in H+ (acidosis) • Causes include: • narcotic overdose, • head injuries, neurological/muscle disease, • severe COPD,
Respiratory alkalosis
Respiratory alkalosis: • Hyperventilation (increased rate and depth of breathing) • Excessive Carbon dioxide removal • causes a reduction in plasma carbon dioxide
↓CO2 + H2O H2CO3 HCO3- + ↓ H+
• Equation moves to left • Leads to an decrease in H+ (alkalosis) • Causes of hyperventilation include: • Panic attack • Hyperventilation due to low O2 levels … e.g. Pulmonary embolism
Metabolic acidosis
Metabolic acidosis: • Extra acid formed /added to body – Diabetic ketoacidosis, lactic acidosis etc. • Or excessive loss of HCO3- from the body (GI or renal)
• Excess of H+ • Equation moves to left More CO2 formed, HCO3- drops • Increased H+ stimulates peripheral chemoreceptors • The CO2 formed (+ more CO2) breathed out respiratory compensation
Metabolic alkalosis
Metabolic alkalosis: • Loss of acid from body (prolonged vomiting etc.)
• Increased HCO3- retention by kidney
• loss of H+ • Equation moves to right CO2 used up; More HCO3- formed, • Low CO2 detected by chemoreceptors, corrected by hypoventilation • But amount of hypoventilation is limited as PO2 cannot drop too much, so very limited resp. compensation
CO2
Renal Compensation for respiratory acidosis and respiratory alkalosis
pH is determined by the ratio of [HCO3- ]: [CO2] in the plasma (20:1)
Renal compensation of Respiratory acidosis
• Kidney reabsorbs all filtered HCO3• It also generates extra HCO3• For every extra HCO3- which enters blood one H+ excreted • HCO3- level rises, • Ratio returns towards 20:1 • pH returns towards normal (both CO2 and HCO3 are high but ratio normal)
insert equations when watching panopto
Renal compensation of Respiratory alkalosis
• Kidney excretes the filtered HCO3• Also stops generating new HCO3-& excreting H+ ions • HCO3- level drops • Ratio returns towards 20:1 • pH returns towards normal (both CO2 and HCO3-are low but ratio normal)
recovery and creation of HCO3
slide 8 lec 1
The anion gap
• Total anions = Total cations • But not all anions and cations are measured
• Difference between measured cations and anions = the anion gap
• ([Na+] + [K+]) – ([Cl-] + [HCO3-]) = Normally 10 – 18 mmol/L
Example: Na+ =140, Cl-=110 K+ =4, HCO3-= 24
Then (140 + 4) – (110 + 24) = 10 mmol/L
This 10 mmol/L are unmeasured anions like SO4–, phosphate, lactate, & protein anions present in the blood.
• Increased anion gap seen in metabolic acidosis (some types)
where extra acid is generated (or added to the body) e.g. • In DKA – Ketoacids ( anion: acetoacetate ) • In hypoxia –lactic acid ( anion: lactate) • In AKI /CKI – retention of acids normally excreted by kidney
• the metabolic acid (e.g. lactic acid) reacts with HCO3- , so HCO3 level drops.
Example: patient with hypoxia, with extra lactate in blood. • cations (148 + 5) = anions (110 + 15 + A- ) A- = all unmeasured anions • 153 – 125 = anion gap is 28 (higher than normal, as extra lactate is included)
Metabolic acidosis with a normal anion gap
• Due to GI or renal loss of HCO3• HCO3- is low but this is replaced by Cl- (HCO3- low, but Cl- high)
• Hence, the anion gap is unchanged e.g. renal tubular acidosis)
Acidosis & hyperkalaemia
Changes in ECF pH causes reciprocal shifts of H+ and K+ between the ECF & ICF
In all cells (muscle, liver, kidney etc)
Acidosis shift of H+ into cells Reciprocal K+ shift out of the cells to ECF
Acidosis leads to hyperkalaemia
In kidney this reciprocal K+ shifts out of the principal cells low intra cellular K+
Hence renal K+ secretion is reduced Potassium is retained Contributing to the hyperkalaemia
Similarly, changes in ECF [K+] causes reciprocal shifts in K+ and H between the ECF & ICF In all cells (muscle, liver, kidney etc)
Hyperkalaemia shift of K+ into cells
Internal balance
Reciprocal H+ shift out of the cells
Hyperkalaemia leads to acidaemia
In kidney this reciprocal H+ shifts out of the intercalated cells intra cellular alkalosis
Hence less H+ secreted by intercalated cells , less HCO3 is reabsorbed / generated Contributing to the acidaemia
Alkalosis and Hypokalaemia
Changes in ECF pH causes reciprocal shifts of H+ and K+ between the ECF & ICF
In all cells (muscle, liver, kidney etc)
K+ H+H + K+
Internal balance
Alkalosis shift of H+ out of cells Reciprocal K+ shift into the cells Alkalosis leads to hypokalaemia
In kidney this reciprocal K+ shifts into the principal cells high intra cellular K+ Hence renal K+ secretion is increased Potassium is lost Contributing to the hypokalaemia
Similarly, changes in ECF [K+] causes reciprocal shifts in K+ and H between the ECF & ICF In all cells (muscle, liver, kidney etc)
Hypokalaemia shift of K+ out of cells
Internal balance
Reciprocal H+ shift into the cells
Hypokalaemia leads to alkalaemia
In kidney this reciprocal H+ shifts into intercalated cells intracellular acidosis
Hence more H+ secreted by intercalated cells , more HCO3 is reabsorbed / generated Contributing to the alkalaemia
peripheral chemoreceptors and centra chemoreceptor changes
slide 17 panopto and slide 18 and 19
Some disease states leading to acidosis/ alkalosis
• Panic attack increased ventilation (hyperventilation) driven by higher (emotional ) centres low pCO2 (respiratory alkalosis) acts on central chemoreceptors to ↓ ventilation, but higher centres overrides this to continue hyperventilation low pCO2 & respiratory alkalosis
• High altitude low inhaled pO2 hypoxia stimulates peripheral chemoreceptors hyperventilation low pCO2 & respiratory alkalosis, some improvement of pO2
• Lactic acidosis (e.g. septic shock due to pneumonia) ↑ [H+] ions stimulate peripheral chemoreceptors hyperventilation low pCO2 (respiratory compensation of metabolic acidosis)
• Lung fibrosis (or pulmonary oedema) Diffusion defect low pO2, but pCO2 normal (since CO2 more soluble, diffuses more easily than O2) hypoxia stimulates peripheral chemoreceptors increased ventilation pCO2 normal or low,
some ↑ in PO2, but hypoxia persists Type 1 respiratory failure (with a degree of respiratory alkalosis, if pCO2 is low)
• Respiratory muscle failure (e.g. Myasthenia gravis) HYPOVENTILATION both hypoxia & hypercapnia
stimulates both peripheral and central chemoreceptors (synergistic effect)
increased neural responses from respiratory centre but unable to increase ventilation because problem at NMJ muscles unable to respond
Type 2 Respiratory failure low pO2, high pCO2 Respiratory acidosis
• Similar course of events in other causes of hypoventilation with type 2 resp failure e.g:
Narcotic overdose Resp centre depressed reduced rate and depath of ventilation hypoventilation low pO2, high pCO2 stimulates both peripheral and central chemoreceptors (synergistic effect)
but respiratory centre unable to respond appropriately hypoventilation persists (Type 2 Respiratory failure Respiratory acidosis)
• Chronic severe COPD when widespread airway narrowing Hypoventilation of entire lung Chronic type 2 Resp. failure
both chronic hypoxia & hypercapnia both peripheral and central chemoreceptors are stimulated increased ventilation some improvement in pO2 and pCO2 but a degree of hypoxia and hypercapnia persists, to which the body acclimatises
(eg. EPO ↑Hb ; renal compensation of respiratory acidosis etc.)
• In Chronic hypercapnia can result in “reset of central chemoreceptors” the hypoxia acting via peripheral chemoreceptors is responsible for the increased rate and depth of ventilation that is needed
• Pneumonia V/Q mismatch in part of lung hypoxia (& initial hypercapnia) initially stimulates both peripheral & central chemoreceptors hyperventilation
hypoxia not corrected, but pCO2 returns to normal or below normal the persistent hypoxia stimulates peripheral chemoreceptors hyperventilation continues low pO2 persists, but normal or low pCO2
Type 1 respiratory failure Respiratory alkalosis (if pCO2 is low)
• Similar course of events in other causes of V/Q mismatch (e.g Pulm. Embolism, acute
asthma etc)
Respiratory failure
• Type 1 Respiratory failure – hypoxia only - pO2 low, pCO2 normal or low 1. Ventilation/Perfusion mismatch
2. Diffusion defect –
• Type 2 respiratory failure - pO2 low, pCO2 high
• Hypoventilation
• NB: Type 1 may progress to Type 2 as disease progresses
• More than 1 mechanism ( eg. V/Q mismatch + diffusion defect) may be operating
Lobar pneumonia
Features on CXR • Opacity corresponds to affected lobe • Non - homogeneous opacity • Air bronchogram may be present
Air bronchogram
Air outlining the branches of the bronchial tree
Pleural effusion
Pleural Effusion • Homogenous density • Density in dependent portion • Curved upper margin (meniscus) • Upper margin higher laterally than medially (yellow arrows on image on right) • Lack of identifiable left diaphragm before and visible diaphragm after clearance of fluid
If large effusion - Mediastinal shift may be present
Differentiating between consolidation in lower zone (lobar pneumonia) and pleural effusion
Lobar pneumonia • Opacity corresponds to affected lobe • Non - homogeneous opacity • Upper border not curved • Can see outline of diaphragm
Pleural effusion - • Fluid always collects in the most dependant part – opacity is in lower zone • More dense, Homogeneous opacity • Upper border curved (meniscus) • Cannot see outline of diaphragm
Pneumonia vs Pleural effusion
Pneumonia
Pneumonia: Inflammatory exudate is inside alveoli, pleural space is clear
Pleural effusion: Fluid is in the pleural space; Alveoli are clear
Lobar pneumonia versus Pulmonary TB (active)
Lobar pneumonia
Acute illness – days High fever Cough with purulent sputum (± Haemoptysis) Pleuritic chest pain Breathlessness
Pulmonary TB
Chronic illness – weeks, months Malaise, weight loss Low grade fever Cough with scanty mucoid sputum, Haemoptysis ± High risk group
Pulmonary T and how its diagnosed?
Pulmonary TB
• Apex often involved
• Ill defined patchy consolidation
• Cavitation usually develops within consolidation
• Healing results in fibrosis
How can active pulmonary TB be diagnosed?
By demonstrating:
• Positive sputum smear for acid fast bacilli (using Ziehl –Nielson stain)
• Positive culture for TB bacilli
• Nucleic acid amplification tests (esp for smear positive patients)
This man has a permanent pacemaker. The pacing wires were introduced via subclavian vein What complication is seen on the CXR?
slide 38
Pneumothorax • Affected side (right) is hyperlucent (darker) • with absent lung markings • Edge of collapsed lung seen (arrows)-lung
collapses towards hilum
• No tracheal shift because it is a non-tension
pneumothorax
Tension pneumothorax vs pneumothorax
inser slide 39 with text
Diaphragm normal position
Diaphragm – normal position
Surface marking In a live person: (at end of quiet expiration)
Dome of R/hemi diaphragm = level of 4th ICS anteriorly (some sources 5th rib anteriorly)
Dome of L/ hemi diaphragm = level of 5th ICS anteriorly
Percussion note: dull below this level
On a Chest x-ray (because CXR taken in deep inspiration)
diaphragm crosses the Anterior part of 6th rib
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Hyperinflated lungs (Asthma, COPD) vs Pneumothorax
inset slide 41
Compare the two x-rays
slde 42 images
whole of slide 42
Portions of the respiratory tract and how cells lining each part change
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The ALVEOLUS & SURFACTANT
Surfactant: Lines alveoli Mix of phospholipids and lipoproteins Diminishes the surface tension of the water film that lines alveoli Thereby decreasing the tendency of alveoli to collapse and the work required to inflate them
Dead space, pulmonary ventilation and alveolar ventilation
Anatomical dead space = The volume of air in the conducting airways
Alveolar dead space = air in alveoli which do not take part in gas exchange (These are alveoli which are not perfused or are damaged) - in a healthy adult alveolar dead space can be considered negligible.
Physiological dead space = anatomical dead space + alveolar dead space = the volume of ventilated air that does not participate in gas exchange
Tidal volume – amount of air inspired and expired at rest– usually about 500 ml of which ~ 350 ml occupies dead space
Total Pulmonary Ventilation (Minute ventilation)= Tidal volume x respiratory rate
Alveolar ventilation = (Tidal volume – Dead space) x respiratory rate
Chronic bronchitis – airways disease
• Chronic bronchitis is a disease of the airways – from bronchi to bronchioles • Mucus hypersecretion (from goblet cells & sub mucus glands) • Reduced cilia – mucus is not cleared effectively • Effects of above lead to • airflow limitation/obstruction by luminal obstruction of small airways • epithelial remodeling, • alteration of airway surface tension predisposing to collapse • Clinical diagnosis – cough productive sputum > three months of the year for > one year
Causes of excessive mucus in chronic obstructive pulmonary disease
slide 51
COPD- Emphysema – air sacs disease
Definition:
Abnormal, permanent enlargement of the air spaces distal to the terminal bronchiole
With destruction of alveolar walls (No fibrosis)
Inflammatory cells accumulate; which release elastases and oxidants destroy alveolar walls and elastin
Protease mediated destruction of elastin is an important feature
Reduced elasticity is a key problem – airway trapping
Also, large air spaces reduced surface area for gas exchange
CXR for paients with emphysema compared to normal
slide 53
Chronic obstructive pulmonary disease (COPD)
• Chronic Obstructive Pulmonary Disease (COPD) is not one single disease but an umbrella term used to describe chronic lung diseases that cause limitations in lung airflow • People with COPD will have a mix of chronic bronchitis and chronic emphysema – but one person may have more emphysematous lungs (ie more air sacs disease) and one may have more chronic bronchitis type lungs ( ie more chronic sputum production) • Management of COPD includes • Making the diagnosis • Reducing risk factors – smoking cessation • Pharmacotherapy for COPD is used to decrease symptoms and complications – inhalers and/or oxygen • Manage exacerbations
What is Bronchiectasis
• DEFINITION: Chronic IRREVERSIBLE dilatation of one or more bronchi – it is a pathological condition that can be caused by many diseases or be idiopathic- resulting in abnormally enlarged bronchi • These deformed bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection
• AETIOLOGY: variety of underlying causes, with a common underlying mechanism of of chronic inflammation • Inflammation causes destruction of the elastic and muscular components of the bronchial wall and peribronchial fibrosis • RADIOLOGICAL FINDINGS • CXR - usually abnormal but inadequate in the diagnosis or quantification of bronchiectasis/ bronchial dilatation
• Gold standard diagnostic investigation = CT - specifically High Resolution CT • We find - bronchial dilatation bigger than the adjacent blood vessel, bronchial wall thickening
slide 56
Bronchiectasis Management
- PHYSIO / AIRWAYS CLEARANCE – Daily airway clearance is essential for treatment success – • Aerosolised saline solutions • Smoking cessation
- Sputum sampling – routine culture and NTM
- Exclude immunodeficiency / treat identifiable causes
- Consider long-term therapies at future visits
- Annual Flu & routine vaccinations against Haemophilus influenzae and Streptococcus pneumoniae
- An established MDT is key
- Management plan for infective exacerbations
Differentiating chronic bronchitis, bronchiectasis, asthma, emphysema and bronchiolitis
slide 58
Ventilation and perfusion
Gas exchange optimal when: • V/Q ratio of individual alveolar units ≈ 1
• 300 million alveoli - may have widely differing amounts of ventilation and of perfusion.
• Ideally, • Alveoli with ventilation should have perfusion
• Alveoli with ventilation should have perfusion
• When pulmonary capillary PaO2 is low, hypoxic vasoconstriction of pulmonary arterioles occurs this diverts blood to better ventilated alveoli • When alveolar PA CO2 is low, bronchoconstriction occurs – This diverts air to better perfused lung • BUT
• This process is not 100% efficient, so in some disease states, poorly ventilated alveoli still have significant perfusion – this is what is meant by ventilation-perfusion MISMatch
Normal physiology of lung ventilation and perfusion
slide 60
Gas composition in a normal alveolus
slide 61
Consequences of Inadequate Ventilation of an alveolar unit
slide 62
V/Q mismatch with V/Q ratio <1
Some causes:
• Asthma (airway narrowing – not uniform throughout lungs • COPD early stages – not uniform throughout lungs • Pneumonia -acute inflammatory exudate in affected alveoli • RDS in newborn -some alveoli not expanded and not uniform • Pulmonary oedema -fluid in alveoli - not uniform throughout lungs
V/Q mismatch is the commonest mechanism causing hypoxia
oxygen-haemoglobin dissociation curve as oxygen partial pressure increases – between 10.6 kPa (80mm Hg) to 16 kPa (120 mmHg)
True or false?
As pO2 increases from 10.6 kPa to 13.3 kPa9 haemoglobin saturation markedly increases by greater than 20%
slide 64 graph
panopto
Graph showing relationship between PCO2 and total CO2 content in blood
slide 65
Relatively straight line in the physiological range pCO2 i.e. there is a linear relationship between pCO2 and blood total content CO2 @ 4-6kPa This is because CO2 Is highly soluble in blood
Unlike O2 it doesn’t require a carrier molecule – remember O2 carrier molecule is Hb
This explains why CO2 in blood is directly proportional to alveolar minute ventilation while O2 is NOT – after a certain point can’t load more haemoglobin with O2 no matter how high pO2
Addiction related to smoking
- Cigarette smoking is a chronic relapsing disorder that starts in adolescence 2. Nicotine causes the addiction, not the harm from tobacco
Markers of Addiction:
• use despite knowledge of harmful consequences • cravings during abstinence • failure of attempts to stop • withdrawal symptoms during abstinence
Physiology of nicotine addiction
- Nicotine acts on nicotinic acetylcholine receptor stimulating dopamine release
- This results in the satisfaction associated with smoking
- Following chronic nicotine exposure, ACh enter upregulated state - increases affinity and functional sensitivity to an agonist
- A drop in nicotine levels leads to craving and withdrawal
- 1-2 puffs of a cigarette binds to 50% ACh receptors
- ACh receptors take between 6-12 weeks to desensitise after the last cigarette
Treating tobacco related disease
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Pharmacological
treatments: nicotine patches/tablets/sprays
E-cigarettes (harm reduction):
• Smoking tobacco kills
• Harm reduction strategy can help those who can’t quit tobacco
• E-cigarettes part of a harm reduction strategy
3 As
Ask - smoking staus
Advise patients of health benefits of quitting
Act on a patients response - build confidence, give information, refer prescribe, offer nhs stop smoking service.
Arguments for and against nicotine use in smoking cessation
Against • Continued nicotine use • Long term effects unknown • Dual use perpetuates smoking • ‘Renormalise’ smoking • Promotes nicotine in young • Gateway to tobacco • Products unsafe • E-cigs made by tobacco companies • Joint marketing of tobacco & ecigs
For • Nicotine is a minor health risk • Negligible compared to tobacco • Quit rates continue to decrease • Normalises E-cigs not tobacco • Compared to tobacco favourable • Experimenters are same group • About to be regulated • Bigger reach for harm reduction • Regulations coming into place
