Respiratory case Flashcards
functions of the respiratory system? (4)
- Gas exchange
- Filtering particle matter
- Defense against inhaled particles and pathogens
- Processing of endogenous compounds by the pulmonary vasculature
Emergency assessment: A B C D E F
AIRWAY BREATHING CIRCULATION DISABILITY EXPOSURE don't ever FORGET to measure blood glucose
Emergency assessment: BREATHING
- What to do:
- Normal:
- Tachypnoea:
- Apnoea:
- Count the number of breaths per minute
- Normal: 10-15 breaths per min
- Tachypnoea: rapid breathing rate
- Apnoea: breathing arrest
Emergency assessment: Look for
- Abnormal blue-purple discolouration of the mucus membranes particularly the tongue
- Abnormal patterns of breathing
Abnormal breathing patterns:
- Keyne-stokes:
- Kussmaul:
- Cheyne-Stokes: often occurs towards the end of life.
- Fast shallow breathing followed by slow deep breathing
- Kussmaul breathing: indicates increased acidity of arterial blood (e.g. diabetic ketoacidosis)
- Deep, rapid and laboured breathing
Auscultating: listening to the breath sounds using a stethoscope
- Normal sounds
- Abnormal sounds
- Normal sounds are known as vesicular
- Abnormal sounds include; wheeze, stridor and bronchial breathing
Abnormal auscultation sounds: stridor
- High-pitched, musical breathing sound
- Caused by a blockage in throat or larynx
Abnormal auscultation sounds: bronchial breathing
- Loud, harsh breathing sounds. Midrange pitch
Hypoxia definition:
- Inadequate oxygen supply to maintain homeostasis in tissues
Hypercapnia:
- Increased arterial pressure of CO2 (PaCO2)
Normal blood oxygen saturation (SaO2):
- 95-100% saturation
Nasopharynx function: (2)
- Function
- Protective reflex
- Warms, humidifies and filters air
- Sneezing is a protective reflex
Laryngeal function: (3)
- Phonation
- Closing the airway during swallowing
- Cough reflex
dead space:
- Volume of gas in respiratory tract that is not involved in gas exchange
- Physiological
- Anatomical
Physiological dead space:
- Anatomical deadspace plus the volume of gas in alveoli that have inadequate perfusion
Anatomical deadspace:
- Volume of gas in upper airways and the conducting zone of the airways
Closing capacity:
- Definition
- Age
- Equation
- Maximal lung volume where airway closure can be detected in the lungs during expiration
- Increases with age
- CC = CV + RV
Factors affecting airways resistance: (2)
- Contraction of bronchial smooth muscle
- Closing capacity
Control of bronchial smooth muscle: neural pathways
- Parasympathetic:
- Sympathetic:
- Postganglionic parasympathetic fibres release acetylcholine, agonising M3 muscarinic receptors
- Causes bronchoconstriction
- NANC: bronchodilator
Control of bronchial smooth muscle: humoral control
- Elevated adrenaline levels in blood agonise beta2-adrenoceptor
- Causes bronchodilation
Control of bronchial smooth muscle:
- Physical effects
- Chemical effects
- stimulation of the respiratory epithelium can cause bronchoconstriction (cold air, dust, smoke)
- Gastric acid aspiration and gas inhalation cause bronchoconstriction
Control of bronchial smooth muscle: local cellular mechanisms
- Inflammatory cells in the lungs (mast cells) may be activated by pathogens or allergens
- Causes bronchoconstriction
Flow/volume loop measured using a spirometer:
- Starts at residual volume (RV)
- Inhales to fill lungs to Total Lung Capacity (TLC)
- Maximum effort to exhale to achieve Peak Expiratory Flow (PEF)
Terminology:
- Ventilation (V)
- Perfusion (Q)
- Minute volume (VE)
- Alveolar ventilation (VA)
- V: refers to the flow of respiratory gases
- Q: the flow of blood
- VE: tidal volume volume of gas exhaled in one minute
- VA: the amount of fresh gas delivered to the alveoli per minute
Minute volume (VE) equation:
VE = tidal volume x respiratory rate
Alveolar ventilation rate (VA):
VA = (tidal volume - physiological dead space) x respiratory rate
Surface tension:
- Alveolus lining
- Bubble
- Cohesive forces
- transmural pressure
- Alveolus is lined with a thin film of fluid
- Behaves like a bubble
- Cohesive forces between water molecules attempt to reduce the surface area and may favour collapse of the alveoli
- To prevent collapse a transmural pressure is required that is predicted via Laplace equation
Laplace equation:
Transmural pressure=
- Transmural pressure = (2 surface tension) / radius
transmural pressure at Functional Residual Capacity:
- Equation
- P(alv)
- P(ip)
- P(alv) - P(ip)
= 0cmH2O - (-5cmH2O) - At FRC alveolar pressure must be equal to atmospheric pressure (0)
- Intrapleural is below atmospheric (negative)
Intrapleural pressure is below atmospheric, so what?
- A penetrating chest injury will allow air to be sucked in to the intrapleural space
- Lung will collapse causing severe respiratory distress
First breaths: (3)
- High transmural pressure to open alveoli for the first time
- must overcome effects of surface tension and elastin
- Surface tension is reduced by surfactant, produced by pneumocyte
Surfactant in embryo’s:
- Surface tension reduced by surfactant produced by type 2 alveolar cells
- Premature babies may lack surfactant and develop respiratory distress
Mechanics of breathing: compliance
- The distensibility of the lungs and chest wall
- compliance = change in volume / change in pressure
Changes in compliance:
- Fibrotic lung disease
- Emphysema
- Fibrotic lung diseases (restrictive): lead to scarring of the lungs, reducing compliance and FRC
- Emphysema (obstructive disease): results in loss of elastin fibres and increase in compliance and FRC (barrel-shaped chest)
Boyle’s law: pressure is inversely proportional to …..
Pressure is inversely proportional to volume
P = 1/v
Breathing cycle: Inspiration
- Inspiration leads to an increase in thoracic volume and a decrease in alveolar pressure to below atmospheric.
- This sucks in the tidal volume
Breathing cycle: expiration
- Passive process
- Decrease in thoracic volume leads to an increase in alveolar pressure to above atmospheric pressure
- Tidal volume blown out
The work of breathing:
- Respiratory muscles require energy to do work
- Work must overcome resistance of airways and elasticity of tissues/effects of surface tension
- Elastic energy stored during inspiration allows expiration to be passive
Pulmonary circulation:
- Pressure generated by:
- Systolic and diastolic pressures:
- Resistance:
- Blood flow:
- Response of small arteries/arterioles to hypoxia
1- Right ventricle 2- 25/8 3- Lower (pulmonary vascular region) 4- Slightly less than 5 L/min 5- Vasoconstriction
Systemic circulation:
- Pressure generated by:
- Systolic and diastolic pressures:
- Resistance:
- Blood flow:
- Response of small arteries/arterioles to hypoxia
1- Left ventricle 2- 120/80 3- higher (total peripheral resistance) 4- 5L/min 5- vasodilation
Physiological shunt:
- Pulmonary vein
- Thebesian vein
- Effect on PA02 and Pa02
- Effect on venous return
- Some deoxygenated blood drains in to the pulmonary veins from bronchial circulation
- Some deoxygenated blood drains in the coronary circulation (5%) into thebesian veins in to the left ventricle
- PA02 > Pa02
- venous return to left ventricle greater than right
V(A):Q=1
- The amount of ventilation with fresh gas equals perfusion with blood
- End capillary blood is fully oxygenated/arterialized
V(A):Q = 0
- Normal perfusion but complete absence of alveolar ventilation
- End capillary blood remains deoxygenated
- Shunt/venous admixture
V(A):Q = infinite
- Normal ventilation but complete absence of perfusion
- No gas is transferred, this is wasted ventilation, increasing physiological dead space
Effects of gravity on V(A):Q
- More ventilation than perfusion at the top of the lung
- V(A):Q will be higher here, as will PAO2
Advantages of hypoxic vasoconstriction: (2)
- Diverts blood away from poor ventilated alveoli e.g. alveoli full of pus in pneumonia
- In utero: low PAO2 results in a high pulmonary vascular resistance, reversed by first breath via lungs
Disadvantages of hypoxic vasoconstriction:
- Barometric pressure
- COPD
- Barometric pressure decreases with altitude, leading to a fall in PAO2 in the lungs, increasing pulmonary vascular resistance, hypertrophy of the right ventricle generates higher pressure
- COPD can also lower PAO2 and cause right ventricular hypertrophy, right ventricular fails in some patients causing cor pumonale
Cor pumonale:
- Right-sided heart failure due to hypoxic lung disease
- Symptoms: blue bloated appearance
- Alveolar ventilation (VA)
- The amount of fresh gas delivered to the alveoli
- VA = (tidal volume - physiological) x respiratory rate
Alveolar ventilation equations:
PACO2=
PACO2 = PaCO2
= Rate of CO2 by metabolism/ rate of CO2 removal
PACO2 directly proportional to rate of CO2 production by metabolism
PACO2 indirectly proportional
Simplified Alveolar ventilation equation:
PACO2 : Rate of CO2 by metabolism / Rate of CO2 removal by alveolar ventilation
Daltons law:
P(TOTAL)= P1 + P2 + P3 ……
Alveolar gas equation use:
- Used to predict a patients PAO2 depending upon the amount of oxygen they’re breathing
Gas exchange: (3)
- Definition
- Diffusion
- Direction
- Refers to diffusion of O2 and CO2 in the lungs and peripheral tissue
- Diffusion occurs due to random thermal motion of molecules
- Gases diffuse down their partial pressure gradient
Diffusing capacity:
- Definition
- Measured by
- Decreased by
- Increased by
- Rate of transfer of gas from alveoli to capillary
- Measured using a single breath with a gas mixture containing a low conc. of carbon monoxide
- Decreased: emphysema, pulmonary oedema, pulmonary fibrosis
- Increased: during exercise(increased capillary perfusion)
Perfusion-limited gas exchange:
- At rest capillary partial pressure of O2 rapidly becomes equal to the partial pressure of oxygen in the alveolus
Diffusion limited gas exchange:
- Caused by lung fibrosis and strenuous exercise
- There is a partial pressure gradient or O2 along the entire capillary, decreasing PaO2
- Greater partial pressure gradient required to increase gas transfer
Calculating the total oxygen content of blood:
C = amount bound to haemoglobin + amount dissolved in plasma
= (O2 binding capacity x SaO2) + (PaO2 x solubility)
Rate of O2 delivery:
O2 delivery = cardiac output (Q) x O2 content (C)
Haemoglobin variants: foetal haemoglobin (HbF)
- Structure
- Affinity
- Lifespan
- Two alpha and two gamma subunits
- Higher affinity for O2 than HbA
- Replaced by HbA within a year of birth
Haemoglobin A (HbA)
- Structure
- Haem moiety
- Bound
- Two alpha subunits and two beta subunits
- Subunits contain a haem moiety, an iron-binding porphyrin with iron in the ferrous state
- Each subunit can bind to one molecule of oxygen
Haemoglobin variants: Methaemoglobin
Iron moiety oxidised to ferric (Fe3+) state
- Does not bind O2
- Congenital form due to deficiency of methaemoglobin reductase
Haemoglobin variants: Methaemoglobin
Iron moiety oxidised to ferric (Fe3+) state
- Does not bind O2
- Congenital form due to deficiency of methaemoglobin reductase
Haemoglobin variants: Haemoglobin S
- Abnormal B subunits
- Sickle cell disease, distorts RBCs causing anaemia
Oxygen Haemoglobin dissociation curve:
- Sigmoidal
- Due to increasing affinity for oxygen with each O2 molecule that binds
- P50 is the PO2 where 50% saturation is achieved
Loading and unloading of oxygen:
- Areas with higher PO2 will have higher saturation, signalling loading
- Areas with low PO2 have lower saturation, signalling unloading
Bohr effect:
- CO2 produced by peripheral tissues results in the generation of H+ ions
- H+ ions bind to HbA, decreasing O2 affinity, facilitating unloading
- In lungs, O2 binding releases H+ ions that react with HCO3- to produce CO2 that is exhaled
Carbon monoxide (CO) poisoning:
- CO binds to HbA with affinity 250 times higher than oxygen
- Decreases O2 binding sites
- Shifts curve to the left, reducing ability to unload O2
CO2 transport in the blood:
- Dissolved in plasma
- Bound to HbA forming carbaminohaemoglobin
- Converted to bicarbonate (HCO3-)
Chloride shift in HbA:
- HCO3- transported out of cell in exchange for Cl- ions
CO2 dissociation curve:
- Linear in shape, CO2 exertion increases with increased ventilation in all areas
Ventilation perfusion mismatch (VQ):
- Defect in the V(A):Q ratio
- Causes arterial hypoxaemia but an increase in alveolar ventilation prevents hypercapnia
Fick’s law: rate of diffusion =
Rate of diffusion (a)
(surface area x concentration) / thickness of membrane
Henry’s law: amount of gas in liquid
At constant temperature, the amount of gas dissolved in a given type and volume of liquid is DIRECTLY PROPORTIONAL to the partial pressure of the gas in equilibrium with that liquid
Control of respiration (PaO2,PaCO2, arterial pH):
- CPG
- A central pattern generator in the brainstem with inputs from the cerebral cortex and multiple types of receptors/sensors
Cerebral (voluntary) respiratory control:
- Voluntary hyperventilation
- Voluntary hypoventilation
If the rate of CO2 production remains constant:
- Voluntary hyperventilation must lead to hypocapnea
- Voluntary hypoventilation must lead to hypercapnia
Respiratory acidosis:
- Hypercapnia drives equilibrium to the right, increasing H+conc. lowering pH
Respiratory Alkalosis:
- Hypocapnia drives equilibrium to the left, decreasing H+conc. raising the pH
Dangers of acute respiratory acidosis: (3)
- Decreased cardiac contractility
- Cardiac arrhythmias and potential cardiac arrest
- Alterations in pH dependent biochem pathways
Hypocapnia symptoms:
- Reduced cerebral blood flow due to vasoconstriction
Central chemoreceptors:
- Location
- Role of CO2
- Ventral surface of medulla oblongata responds to increases in H+
- H+ ions cannot cross the blood brain barrier (BBB), CO2 diffuses across the BBB and is converted to H+
Peripheral chemoreceptors:
- Found in carotid sinus
- Stimulated by acidemia, hypoxia, hypercapnia and decreased perfusion (hypotension)
Influence of CO2 on respiratory control: (3)
- Rise effects
- Max
- Min
- A rise in PaCO2 above 5.3KPa causes an incremental rise in minute volume
- Max PaCO2 is 13.3-26.7KPa, after which CO2 narcosis occurs with respiratory fatigue
- Hyperventilation resulting in PaCO2 less than 5KPa can lead to apnoea until levels are restored
Influence of oxygen on respiratory control
- Linear relationship between PaO2 and minute volume until SaO2 drops too far, stimulating a powerful stimulus
Influence of pH on respiratory control:
Arterial pH depends upon ratio of bicarbonate to PaCO2
pH = [HCO3-] / PaCO2
Metabolic acidosis:
- A pathological decrease in [HCO3-] causes a fall in blood pH
- Often seen in uncontrolled type 1 diabetes mellitus
Metabolic acidaemia correction:
- Peripheral chemoreceptors stimulated, increasing alveolar ventilation, decreasing PaCO2
- Reduces pH disturbance
Influence of opioids in respiratory control:
MOP receptors
- Opioids bind the MOP receptors and depress alveolar ventilation
- Pathological rise in PaCO2 causes respiratory acidosis, pH falls
- Reversed using the antagonist naloxone
Cellular respiration:
- Food molecules digested to produce fatty acids, glycerol, amino acids and sugar
- These products are oxidised to form ATP, NADH and other activated carrier molecules
Oxidation of glucose (cellular respiration):
- Cell oxidises glucose in a series of enzyme-catalysed steps, gradually releasing energy which is captured by activated carrier molecules
Glycolysis:
- Major metabolic pathway for sugar oxidation
- Occurs in the cytosol of cells
- 6-carbon glucose is converted into 2X 3-carbon molecules of pyruvate
Glycolysis steps (3):
- Investment
- 6-carbon sugar
- Energy generation
- Energy investment to be recouped of 2 ATP’s to drive unfavourable reactions
- 6-carbon sugar is cleaved into 2X 3-carbon sugars
- Energy generation: two NADHs, two pyruvate and 4 ATPs are formed
ATP functions:
- A building block of DNA, RNA
- Combine with other groups to form coenzymes
- as cyclic AMP, a signalling molecule
ATP functions:
- A building block of DNA, RNA
- Combine with other groups to form coenzymes
- as cyclic AMP, a signalling molecule
Anaerobic energy generation:
- When oxygen is limited pyruvate is converted into lactate (muscle) or ethanol and CO2 (yeast)
- NADH is oxidised to NAD+ to allow glycolysis to continue
Metastasize:
Warburg effect:
- Malignant tumours reproduce very quickly
- They consume large amounts of glucose and produce lots of lactate
Glycogen:
- Stores sugars in small granules in the cytoplasm of many cells
- Used during short periods of fasting
Triglycerides:
- Stores fatty acids in adipocyte cells
- Used for longer periods of fasting
- Adipose tissue can be white or brown, brown containing more mitochondria
Liver specialities:
- Use of glucokinase (KM=10mM) as opposed to hexokinase (KM=0.1mM)
- Following a meal, only liver cells can increase their rate of glucose phosphorylation
- G6P in liver cells can be used to synthesise glycogen
Mitochondria:
- Membranes (4)
- Outer membrane permeable to many molecules
- Inner impermeable to all, unless specific transport proteins are present
- Inner membrane is the site for oxidative phosphorylation (ATP synthesis)
Mitochondria function:
- Pyruvate pumped into the mitochondrial matrix and converted into acetyl CoA and CO2 by Pyruvate Dehydrogenase Complex
Citric acid cycle overview:
- Two carbons from acetyl CoA combine with 4-carbon oxaloacetate, forming six carbon citrate
- Citrate is progressively oxidised, producing NADHm FADH2, GTP.
- CO2 is a waste product
Citric acid cycle products:
- 3 NADH
- 1 GTP
- 1 FADH2
- 2 CO2
Oxidative Phosphorylation:
- Uses high-energy electrons in NADH, GTP and FADH2 to produce a concentration gradient of H+ out of the mitochondrial matrix.
- H+ renters the matrix via ATP Synthase channels
Oxidative phosphorylation overview:
- Electrons move across three complexes in the inner mitochondrial membrane
- Pumping protons out of the cell, creating an electrochemical gradient
- ATP synthase uses protons flowing down the gradient to form ATP
How is Vo2 (O2 consumption rate) measured:
- Measured using a spirometer filled with 100% oxygen
Phases of respiration during exercise: (3)
- Phase I: instant increase in ventilation at, or slightly before exercise begins
- Phase II: Further increase to reach phase III
- Phase III: equilibrium level
Oxygen debt:
- During phase II some of the energy required is produced by anaerobic metabolism
- This generates lactate
- During recovery minute volume remains elevated to allow lactate to be metabolised (repaying O2 debt)
Vo2MAX:
- An individuals maximum oxygen consumption rate
- Used as a measure of respiratory fitness
Exercising above Vo2 MAX:
- A subject can exercise at a higher intensity than Vo2MAX via anaerobic respiration
- This produces lactic acid, ionised to H+ and lactate ions
- This causes a rise in arterial pH, stimulating chemoreceptors, causing increases in minute volume and alveolar ventilation
Effects of lactic acid:
- causes a rise in arterial pH, stimulating chemoreceptors, causing increases in minute volume and alveolar ventilation
- Causes distress above levels of 11 mmol/L, a limiting factor for sustained heavy work
Oxygen delivery (O2) =
O2 delivery = Cardiac output (Q) x O2 content (C)
Effects of increased mean pulmonary artery pressure:
- Increases pulmonary blood flow
- Increases perfusion of the lung apices
- Reduces physiological dead space, improves VA:Q
Fick equation and limiting factors of Vo2MAX:
- Vo2MAX= MAX CO X difference in arterial and venous O2 content
Effects of training upon the heart:
Increases: - Myocardial capillaries - Size of ventricular chamber - Vagal tone, resulting in resting bradycardia Results in increased Cardiac output (Q)
Effects of training upon skeletal muscle:
- Increases
- Effects
Increases: - Capillaries - Mitochondria - Myoglobin Allows an increase in oxygen extraction, increasing anaerobic threshold and livers ability to clear lactate
Ergoreflex:
- Mechanoreceptors and metaboloreceptors in skeletal muscle cause an increase in ventilation and HR during exercise
The oxygen cascade:
- Process by which Oxygen partial pressure reduces from 21.2KPa (dry air, sea-level) to 0.5-3 KPa (in mitochondria)
- A pathological disturbance can lead to tissue hypoxia and dysfunction
Normal arterial PaO2:
- PaO2 = 13.6 (0.044 x age)
Hypoxaemia:
- Abnormally low arterial partial pressure of oxygen (PaO2)
- Associated with central cyanosis (blue tongue)
Hypoxia:
- Low tissue partial pressure of oxygen
- Hypoxaemia is one cause of tissue hypoxia
Causes of hypoxaemia: (5)
-Compared how?
Five possible pathological causes: - High altitude - Hypoventilation - Diffusion defect - VA:Q mismatch - R to L cardiac shunt Compared by their effects on Alveolar-arterial difference Aa Dif. = PA02 - PaO2
Hypoxaemia causes: High altitude
- Notes
- PaO2 effect
- Aa difference
- Does O2 help?
- Fall in barometric pressure leads to a decrease in PIO2 and PAO2
- Decrease
- Aa normal
- Yes
Hypoxaemia causes: Hypoventilation
- Notes
- PaO2 effect
- Aa difference
- Does O2 help?
- Decreases PAO2
- Decreases PaO2
- Aa normal
- Yes
Hypoxaemia causes: Diffusion defect
- Notes
- PaO2 effect
- Aa difference
- Does O2 help?
- Decreases PaO2
- Increased Aa difference
- Yes
Hypoxaemia causes: VA:Q mismatch
- Notes
- PaO2 effect
- Aa difference
- Does O2 help?
- Decreases PaO2
- Increased Aa difference
- Yes
Hypoxaemia causes: R-to-L cardiac shunt
- Notes
- PaO2 effect
- Aa difference
- Does O2 help?
- Shunted blood bypasses the alveoli and cannot be ventilated, resulting in very low PaO2
- Decreased
- increased Aa difference
- Limited effect only on non-shunted blood
Causes of tissue hypoxia: Stagnant hypoxia
- Decrease in cardiac output causes a decrease in rate of O2 delivery
Causes off tissue hypoxia: Hypoxaemia
- A decrease in SaO2 and PaO2 reduces total O2 content, reducing rate of O2 delivery
Causes of tissue hypoxia: anaemic hypoxia:
- Concentration of haemoglobin falls, lowering oxygen binding capacity, which lowers O2 content
Causes of tissue hypoxia: histotoxic hypoxia:
- An inability of the cells to utilise oxygen
Hypoxia symptoms: _ A - E - C/L of C - T - U/C/S
- Anxiety
- Euphoria
- Confusion/lack of coordination
- Tachypnoea, use of accessory muscles
- unconsciousness/coma/seizures
Pressure of inspired air (PIO2)
- FIO2
- PB
- PH2O
PIO2 = FIO2 x [PB - PH2O]
FIO2= fractional O2 composition PB = Barometric pressure PH2O = Water vapour pressure
The challenge of high altitude:
PIO2 = FIO2 x [PB - H2O]
- At high altitudes PB falls, lowering PIO2
Acclimatisation:
- Definition
- Respiratory changes
- increase in tolerance to high altitude when subject gradually ascends to high altitude
Ventilatory changes: - Polycythaemia (Increase in Hb)
- Hypoxic vasoconstriction, increases PVR
- Raised pulmonary artery pressure and R.ventricular hypertrophy
Acute altitude sickness:
- Symptoms
- Treatment
- Headaches, anorexia, insomnia
- Evacuate patient to lower altitude
