Kanani: Surgical Critical Care Flashcards
What does Henry’s law state, and how is this used to calculate the amount of oxygen dissolved in the blood?
Henry’s law states that the gas content of a solution is equal to the product of the solubility and the partial pressure of the gas.
At 37°C the solubility of oxygen in blood is 0.03 ml/L for every mmHg rise in the partial pressure (0.03 ×PaO2).
What is haemoglobin composed of?
4 Haem component: Fe2+ and protoporphyrin ring
4 Globin chains: 2 alpha, 2 beta chain + 2,3-bisphosphoglycerate
Haemoglobin can bind with 4 oxygen molecules = 8 oxygen atoms
What other molecules may bind to a haemoglobin under normal circumstances?
- Carbon dioxide (CO2): binds to globin chain forming carbamino compound
- Protons (H+): bind to amino, carboxyl and imidazole groups in globin chain
- 2,3-BPG: by-product of red cell metabolism, forms covalent bond with beta subunits, wedging them apart in de-oxygenated state
What are the main sites of haemopoesis?
- Yolk sac: in first few weeks of gestation
- Bone marrow: from first few weeks after birth
- live and spleen: important until c.7mo gestation, in adulthood may revert to these sites in pathological states -> extramedullar haemopoesis
Life span for RBC
120 days -> broken down by reticuloendothelial system
Draw the oxygen dissociation curve and label the axis
Co-operative - binding of 1 molecule facilitates binding of the next -> Sigmoidal due to progressive nature with which each O2 molecule binds Haemoglobin
Bohr Effect - shift of dissociation curve to the right, signifying a reduction in affinity to oxygen, i.e. a tendency to off-load O2 into the tissues. Caused by:
- increased temp
- increased acidity
- increased 2,3-BPG (e.g. chronic hypoxia)
- hypercarbia
This ensures O2 is more readily available during states of acute/chronic reduction in O2 perfusion
NOTE: CO2 dissociation curve is curvilinear
How does the oxygen dissociation curve in the foetus compare of that of the adult and what accounts for this difference?
Foetal oxygen dissociation curve is shifted to the left reflecting increased O2 affinity of foetal haemoglobin caused by the presence of the gamma (rather than beta) subunit that cannot form covalent bonds with 2,3-BPG. This ensures it is readily available to take up O2 from maternal Hb molecule
How much oxygen is bound to haemoglobin when fully saturated?
What factors does the total amount of oxygen in the blood depend? How is this calculated?
When fully saturated each gram of haemoflobin can bind to 1.34ml of oxygen.
Oxygen carrying capaciy of blood = 1.34 x [Hb] at full (100%) saturdation
O2 content = amount bound to Hb + amount dissolved in blood
= 1.34 x [Hb] x % saturation + 0.03 x PaO2
Factors:
- [Hb]
- % saturation
- PaO2
- Temp (which determines O2 solubility)
What’s the FiCO2 of atmospheric air
0.00035 = 0.035%
What is the alveolar-arterial pCO2 difference?
Virtually none due to high water solubility of CO2 compaired to O2 -> CO2 rapidly diffused across resp epithelium
The difference increases under pathological conditions of V/Q mismatch and when there is increased CO2 production
How is CO2 transported in the body?
- Bicarbonate ions (HCO3-): 85-90% of carriage
- Carbamino compounds: 5-10% of carrigae - CO2 binds with terminal amino groups of plasma proteins (including haemoglobin)
- Dissolved in solution: 5% (compared to c.1% of O2)
In arterial blood: Less carbamino compound carriage and more bicarbonate carriage (due to difference in pH affecting the binding/dissociation properties)
How does CO2 come to be carried as the bicarbonate ion?
CO2 + H2O = H2CO3 = H+ + HCO3-
Catalysed by carbonic anhydrase
H+ is mopped up by other buffer systems e.g. binds with the imidazole group of the polypeptide chain in haemoglobin
The H+ and CO2 binding to the haemoglobin chain -> R shift in oxygen dissociation curve -> reduced affinity to O2
What happens to the bicarb generated in the red cell when it carries CO2?
The HCO3- diffused out of the red cell into plastma (unlike H+, it is able to penetrate the red cell membrane)
Electrochemical neutrality is maintained by the chloride shift - CL- enters as HCO3- leaves
The bicardb and chloride generated following CO2 carriage by RBC -> increased osmotic pressure -> H20 diffusion in -> 3% higher haematocrit in arterial blood
Why cannot the amount of CO2 in blood be expressed in %-saturation unlike the case for oxygen?
Because CO2 is more water soluble than oxygen and never reaches a saturation point!
Difference between the Bohn effect and the Haldane effect?
Bohr Effect - changes in affinity of haemoglobin chain for oxygen following variations in PaCO2 H+ temp
Haldane effect - changes in affinity of blood for CO2 as PaO2 changes - as PaO2 increased, affinity of blood for CO2 decreases (downward shift)
What is the relationship between PaO2 and PaCO2?
Alveolar gas equation
PaO2 = PiO2 - PaCO2 / R
PiO2 = inspired pO2
R = respiratory exchange ratio = 0.8
How may O2 be delivered to the patient?
- Variable performance devides: FiO2 delivered depends of flow rate e.g.:
- Nasal cannulae
- Face mask/Hudson mask: ;at 2L/min, FiO2 achieved = 0.25-0.3, At 6-10L/min FiO2 = 0.3-0.4
- Fixed performance devices: constant FiOs delivered
- Venturi: O2 flows through a device that entrains air from side holes at a certain rate, degree of air mixing determines FiO2
- Resevoir bag/non-re-breath mask: attached to end of facemask. Patient inhales directly from O2 in bag therefore FiO2 is close to 1.0
- Continuous positive pressure ventilation: positive pressue is delivered throughout the respiratory cycle ensuring small airways don’t collapse at the end of expiration e.g. pulonary oedema, pneumonia, OSA
- BiLevel Positive airway pressure/Non-invasive ventilation: provides 1 pressure level of inhalation and 1 for exhalation, drives ventilation e.g. COPD/hypercapnic resp failure/weaning tracheal intubation
- Invasive respiratory support: requires intubation to enable intermittend positive pressure ventilation
FiO2 of atmospheric air = 0.21
What are the dangers of oxygen therapy?
- In chronic retainers
- Loss of hypoxix pulmonary drive -> apnoea
- Loss of hypoxia reverses normal compensatory hypoxic pulmonary vasocontriction -> deteriorating V/Q mismatch
- Absorption atelectasis: absence of nitrogen, which by slow absorption splints the airways open, airways collapse after rapid O2 absorption in the alveoli
- Pulmonary toxicity: O2 irritates the mucosa of airways -> loss of surfactant -> fibrosis
- Risk of fires/explosion: O2 supports combustion
What is pulose oximetry and what does it measure?
Non-invasive continuous method of assessing SaO2 and pulse rate
Finger tip and ear lobe = most common sites
Does NOT measure total oxygen or PaO2
Does NOT assess ventilation - which requires PcAO2 meaurement
Uses spectrophotometry - LEF at red 660nm and infra-red 940nm wavelengths on a photodetector (photodiode) - differing amoounts of light absorbed by saturated and unsaturated Hb molecules - % O2 saturation is calculated from the ratio between these 2 forms of the molecule
Issues:
- Diminished accuracy below 70% saturation
- 20secs delay between actual and siplayed values
- in poor peripheral perfusion ambiant light pollution leads to poor signal quality
- Abnormal pigments affect the results e.g. external: nail varinish, internal: bilirubin (underestimates), methaemoglobin, carboxyhaemoglobin (over-extimates)
- Abnormal pulsations e.g. arrhythmias/benous pulsations of R heart valve defects may intefere with the signal
What is methaemoglobin?
Haemoglobin containing iron in the ferric Fe3+ state within the haem portion (as opposed to ferrous Fe2+ state)
- congenital deficiency in reducing enzymes
- Acquired e.g. exposure to LA prilocaine
Carry less O2 -> cyanotic (darker colour)
Rx - reducing agent e.g. methylene blue
How may ventilation be assessed?
Measured by ability to ‘blow off’ CO2 adequately
Therefore measure by capnography - end tidal CO2 detected by sensory in exhaled stream of air = good measure of PaCO2 when VQ is well matched due to high solubility of CO2
Capnography therefore useful for measuring airway patency & detection of oesophageal intubation
Airway adjuncts
Overcome soft palate obstruction and backward tongue displacement
Nasopharyngeal airway - bevelled end & stopped at other end
- tolerated in conscious patient
- CI in base of skull/cribriform plate fractures
- 6-7mm
- SE: damage nasal mucosa, nasal bleeding, laryngeal/glossopharyngeal reflexes -> laryngospasm and vomiting
- How? Check right nostril patency, lubricate tip, insert bevel end first and perpendicular to orifice (towards ear). Oncer in place re-assess airway (look listen feel)
Oropharyngeal airway - curved plastic tuve, flanged and reinforced at the oral end, stopped flattened so teeth can bite into it
- Not tolerated in conscious patients
- Insertion contraindicated if gag reflex is present, if tolerated = significant decreased in GCS and imminent airway compromise
- sizes: SML,2/3/4
- SE: insertion may push the tongue back, exacerbating obstruction, lodge the vallecular/epiglottis, laryngospasm and vomiting may occur if inserted in conscious patient (glossopharyngeal and laryngeal reflexes present)
- How? Open mouth employing basic airway menourvres. Suction out debris, insert upside down (curved side pointing the palate) Rotate 180 between hard and soft palate and seat the flattened section between gums and teeth
What kinds of surgical airway are there?
- Needly cricothyroidotomy
- Cricothyroidotomy
- Tracheostromy, emergency or elective
What are the indications for a surgical airway?
- Failed intubation, due to oedema
- Traumatic fracture of larynx
In which anatomical location are the surgical airways sited?
Cricothyroidotomy: Median cricothyroid ligament - Thickened anterior portion of the cricothyroid membrane - runs between cricoid and thyroid cartilate
Tracheostomy: from 2nd-5th tracheal rings
How is jet insufflation of O2 performed, and what is the main precaution to be considered?
Needle passed into airway through median cricothyroid ligament
Connected to source of O2 via tracheal tube connector
Oxygenate but poorly ventilated -> progressive hypercarbia
Limitted to <45mins
Need to obtain definitive airway
How can you assess respiratory function?
Non-invasive:
- Peak expiratory flow rate (PEFR): bedside measure of airway resistance and resp muscle function
- Pulse oximetry: arterial oxygen saturation (SaO2) and HR
- Capnography: end-tidal CO2
- Pulmonary function tests:
- Spirometry - lung volumes e.g. Functional expiratory volume in 1 second (FEV1), functional vital capacity (FVC), FEV1/FVC (normally >80%), Total lung capacity (TLC), Residual volume (RV)
Invasive:
Which investigations can be used to assess cardiovascular function?
Non-invasive:
- Pulse: clinical assessment of rate, rhythm e.g. radial artery, volume, character e.g. carotid artery
- Non invasive BP: sphygmomanometer
- Electrocardiograph (ECG) - rate, rhythm, intervals, axis, waveform
- Transthoracic echocardiography (TTE): systolic function, cardiac filling, valve function, morphology, blood flow
- Radiology: plain chest radiograph (cardiothoracic ratio), CT, MRI
- Clinical: GCS (cerebral perfusion), CRT, urine output
Invasive:
- Intra-arterial BP: e.g. radial arterial line - continuous arterial waveform and beat to beat variations
- Central venous catheter: e.g. internal jugular vein -> Central Venous Pressure
- Pulmonary artery flotation catheter: direct and derived left heart function e.g. cardial output + systemic and pulmonary vascular resistance e.g. pulmonary artery capillary wedge pressure, oxygen delivery, SaO2 and demant
- Transoesophageal echocaridiography (TOE): more detailed picture than transthoracic echo
- Cardiac catheterisation and coronary angiography: gold standard diagnostic procedure re structure and function of heart
- Invasive assessment of cardiac index and peripheral organ perfusion:
- ABG - acidosis and base excess assoc with anaerobic metabolism
- Biochem e.g. serum lactate
Define the blood pressure
BP = CO x SVT
Blood pressure = cardiac output x systemic vascular resistance
CO = HR x SV
Cardiac output = heart rate x stroke volume = 5-6L/min
How can blood pressure be monitored?
Non-invasively e.g. sphygmomanometer
Invasively - direct cannulation of a peripheral artery e.g. invasive arterial blood pressure -> continuous waveform trace after attachement to electronic pressure transducer
How does invasive monitoring compare to non-invasive monitoring?
Invasive blood pressure monitoring e..g radial lines measure SBP/DBP 5/8mmHg higher/lower than non-invasive BP measurement techniques
Advantages:
- Continuous - does not need repeated nurse measurements
- Accurate - even when profoundly hypotensive
- Other - indications re myocardial contractility can be determined from arterial swind of trace
Disadvantages:
- Complications - invasive procedure in artery under high pressure
- Skilled: requires technical skill & fell ASNTT
- Expensive
Draw the BP waveform
The dicrotic notch is a momentary rise in the arterial pressure
trace following closure of the aortic valve.
What is a direct Coomb’s test?
dAg
- used for detection of antibody or complement on the surface of RBC that have developed in vivo
Indirect Coombs
- detection of antibody or complement on the surface of RBC that have developed in vivo
- Haemolytic transfusion reactions
- Haemolytic disease of newborn
- Autoimmune haemolytic anaemia
Draw a typical ECG waveform and label the various reflections
PR - begining of P to begining of QRS complex
QRS - widge of QRS
QT -begining of QRS to end of T
What are J and U waves, where do they occur and under what circumstances?
J wave (Osborn) = upward deflection at the junction of S wave and ST segment, represents hypothermia
U wave = low voltage wave after T wave, prominent in hypokalaemia
What kinds of tachyarrythmias do you know?
- Broad complex:
- Regular: VT or SVT in BBB
- Irregular: AF in BBB, AF in ventricular pre-excitation syndrome e.g. Wolff Parkinson White syndrome, polymorphic VT
- Narrow complex
- Regular: non-pathological sinus tachy and paroxysmal SVT e.g. Atrioventricular re-entry tachycardia (AVRT) WFW syndrome and atrial flutter in regular AV conduction block e.g. 2:1
- Irregular: AF (most common) or A flutter in variable AV conduction block 2:1, 3:1, 4:1
