POSTOPERATIVE COGNITIVE DYSFUNCTION – RISK FACTORS
Category Archives: Anesthesia
PROJECT THE RAYS CORRECTLY: Basic facts about projection in X ray films
A postero-anterior (PA) projectionn will not produce as much magnification of the heart and mediastinum as an antero-posterior (AP) projection. So PA films are the preferred ones. Here the scapula is rotated; so the lung fields are clear.
A PA film is taken with the film cassette in front of the patient and the beam delivered from behind with the patient in an upright position.
Portable films and those taken in ICUs are all AP projection. All anterior structures appear magnified—heart, mediastinum, sternum, clavicles, and ribs
The supine position causes distension of the upper lobe blood vessels, which may be confused with elevated left atrial pressure
A lateral X-ray is useful in viewing retrosternal and chest wall lesions, localising lesions in the AP dimension, locate lesions behind the left side of the heart or in the posterior recesses of the lungs. Lateral decubitus—used in diagnosing very small collection of air or fluid in the pleural space.
A left lateral (with the left side of the chest against the film and the beam projected from the right) is the standard projection.
The heart is magnified less with a left lateral as it is closer to the film.
To visualize lesions in the left hemithorax, obtain a left lateral film and for right-sided lesions a right lateral.
Expiratory films are used to assess air trapping in bronchial obstruction such as a foreign body.
A pneumothorax always appears larger on an expiratory film and occasionally a small pneumothorax may only be visible on expiration.
Films if accidentally taken in expiration, can result in spurious magnifcation of the heart and mediastinum.
- PROJECTION: The different projections of importance to us are Postero Anterior (PA), Antero Posterior (AP), Lateral, Supine, and Lateral decubitus.
- ROTATION: An image is not rotated if the clavicular heads are equidistant to the
corresponding thoracic spine - INSPIRATION: An inspiratory picture shows a ‘lot of lung’. In inspiratory films the
level of the diaphragm is at the level of ribs 5/6 anteriorly and 8/10
posteriorly. (AR6PR10) - PENETRATION: A film is adequately penetrated if the vertebral bodies can be
visualised against the cardiac silhouette
A normal chest radiograph can be summarised as ‘…the trachea is central and the hila are normal. Lung fields are clear with no air or fluid collection. Heart and mediastinum appear normal and not displaced. There is no free air under the diaphragm, and the angles are clear. Also, the bones and soft tissues appear normal…’
–>Before diagnosing a CXR as normal, look at the areas where
pathology is commonly missed.
*Apices (including behind the 1st rib and clavicle)—small pneumothoraces and masses
*Hila—masses and lymph nodes; left hilum is 1–2 cm higher than right
*Behind the heart—left lower lobar collapse and hiatus hernia
*Below the diaphragm—free gas
*Soft tissues—breast shadow or absence (look for lung and bone metastasis)
#xray ,#radiology ,#imaging , #XrayBasics , #anaesthesia
Reference: Radiology for Anaesthesia and Intensive Care (Richard Hopkins, Carol Peden and Sanjay Gandhi)
THE BASICS OF RESPIRATORY PHYSIOLOGY
CO2 is the most important stimulus for respiration
Receptors for CO2 are found in the medulla of the brain (central chemoreceptors)
Receptors for O2 are found mainly in carotid and aortic bodies
CO2 is the more important gas as the body has more capacity to store CO2 than O2 or hydrogen ions
In normal people at sea level, only 10% of the respiratory drive is due to hypoxic stimulation.
Unlike the central stimulation of hypercapnia, hypoxia causes central depression of the respiratory drive.
Acidosis (high H+ / low blood pH) stimulates respiration; conversely alkalosis depresses it.
For gas exchange, the lungs provide an interface of total surface area about 55 m2 via 700 million alveoli
Alveolar ventilation’ is that part of the total ventilation (i.e. all gas entering the lungs) that participates in gas exchange with pulmonary capillary blood; it is equal to total ventilation minus the ventilation of the conducting airways (i.e. dead-space ventilation).The average alveolar ventilation is about 4 L/min.
The alveolar–arterial oxygen gradient ( P(A-a)O2 ) is a measure of the oxygen that has reached the arterial blood supply as a ratio of the total oxygen in the alveoli. It is a useful index of pulmonary gas exchange function.
This requires that three elements are working correctly:
- Circulatory anatomy is normal. Anomalies such as ASD & PDA can cause anatomical shunting, i.e. venous blood passes through routes that are not exposed to alveolar air
- Ventilation and perfusion are matched
- The respiratory membrane allows sufficient free diffusion of gases between air and blood. A diffusion defect impairs the alveolar–capillary membrane, e.g. in interstitial lung fibrosis
In a healthy individual breathing room air (at FiO2 0.21) the PO2 in alveolar air is 104 mmHg and in arterial blood 95 mmHg . PAO2 exceeds PaO2 by 15 mmHg .Thus, at an FiO2 of 21, the P(A–a)O2 is 15 mmHg
In blood, CO2 is present as:
Dissolved in blood plasma (5.3% in arterial blood)
Bound to haemoglobin as carbaminohaemoglobin within erythrocytes (4.5%)
In the form of bicarbonate attached to a base (90%)
Reference:”Understanding ABGs & Lung Function Tests” Muhunthan Thillai, Keith Hattotuwa
Drugs that act as Respiratory stimulants/ depressants
Drugs that act as Respiratory stimulants
Acetazolamide
Aminophyllines
Doxapram
Progesterone
Salicylates
Drugs that act as Respiratory depressants
Alcohol
Anaesthetics
Anticholinergics
Antihistamines
Barbiturates
Benzodiazepines
Opioids
NATURALLY OCCURRING OPIOIDS
MNEMO>
P͎A͎P͎A͎ C͎a͎r͎e͎s͎ M͎O͎R͎e͎ T͎H͎a͎n͎ N͎A͎T͎U͎R͎E͎
PAPAVERINE CODEINE MORPHINE THEBAINE
Do you know what CVS anomaly you have to rule out, if you get a patient with TURNERS SYNDROME, for any surgery?
MNEMO>
Aorta is the vessel, which ‘TURNs back’
Answer: Coarctation of Aorta, Aortic Valvular Disease!!
REFINE YOUR IMPRESSION OF 📕PaO2 Vs 📗SaO2 Vs 📘CaO2
⭕️Oxygen content ( PaO2 ) is the pressure of oxygen molecules dissolved in blood, and is measured by ABG analysis with units of kPa or mmHg
⭕️Oxygen saturation ( SaO2 ) is a measure of the percentage of haemoglobin sites that have oxygen bound, commonly measured with a pulse oximeter
⭕️Oxygen content ( CaO2 ) is the real measure of blood oxygen quantity as it accounts for dissolved and haemoglobin bound oxygen. (i.e. CaO2 directly reflects the TOTAL number of oxygen molecules in arterial blood, both bound and unbound to hemoglobin. It is given as the volume of oxygen carried in each 100 ml blood (mL O 2 /100 mL). Normal CaO2 ranges from 16 to 22 ml O2/dl.
EXPLANATION:
⭕️Oxygen saturation ( SaO2 ) is expressed as the percentage of haemoglobin-binding sites that are occupied by oxygen, thereby forming oxyhaemoglobin.
⭕️Arterial blood is normally at 97–98% O 2 saturation (i.e. 98% of the available haemoglobin is combined with O 2 ), whereas venous blood is normally at 74% O2 saturation.
⭕️O2 constitutes 21% of the atmosphere by volume and atmospheric PO2 is 159 mmHg at sea level . At an alveolar pressure of 104 mmHg, alveolar oxygen diffuses into pulmonary venous blood and raises its O2 content from 15 mL/100 mL to 20 mL/100 mL. Of this amount 19.75 mL is combined with haemoglobin and 0.25 mL is ‘free’ or dissolved in simple solution in the plasma. At this pressure of alveolar O2 , haemoglobin in the arterial blood normally becomes 98% saturated and and 2% of the haemoglobin remains reduced, i.e. free of oxygen.
⭕️PaO2 is determined by alveolar PO2 and the state of the alveolar-capillary interface, not by the amount of hemoglobin available to soak them up. PaO2 is not a function of hemoglobin content or of its characteristics. This explains why, for example, patients with severe anemia or carbon monoxide poisoning or methemoglobinemia can (and often do) have a normal PaO2.
⭕️The most common physiologic disturbance of lung architecture, and hence of a reduced PaO2, is ventilation-perfusion (V-Q) imbalance. Less common causes are reduced alveolar ventilation, diffusion block, and anatomic right to left shunting of blood.
⭕️Think of PaO2 as the driving pressure for oxygen molecules entering the red blood cell and chemically binding to hemoglobin; the higher the PaO2, the higher the SaO2.
⭕️ In contrast to the other two variables, CaO2 depends on the hemoglobin content and is directly related to it; Since the dissolved oxygen contributes minimally to CaO2 under physiologic conditions, CaO2 is determined almost entirely by hemoglobin content and SaO2, and is related linearly to either variable.
CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x (.003 ml O2/mm Hg/dl).
Labetalol Pharmacology
Comes as 5 mg/mL ampoules
Blocks α, β1, and β2 adrenergic receptor sites.
Decreases heart rate and peripheral vascular resistance.
Ratio of alpha to beta blockade depends upon the route of administration (1:3 oral versus 1:7 IV)
Onset of action: 2‐5 minutes
Will not cause bronchoconstriction
Duration: 2‐4 hours
IV Bolus: 20 mg over at least 2 minutes as initial dose, may repeat with doses of 40-‐ 80 mg q10min; Do not exceed total dose of 300 mg
Infusion [ dilution 1 mg/mL] : starting 2 mg/min (2 mL/min) – 8 mg/min titrated to response. Do not exceed total dose of 300
As cumulative dose nears 300mg IV, duration of action extends to nearly 18 hours.
Ref: B Xu, F Charlton, A Makris, A Hennessy – Journal of hypertension, 2014
HYPOPHOSPHATAEMIA IN ICUs
Normal range (2.5-4.5 mg/dL),
Hypophosphataemia = phosphate concentration < 2.5 mg/dL or 0.81 mmol/L
CAUSES:
Poor Nutrition
Chronic Alcoholism
Diarrhoea
Beta 2 Agonists
Insulin Acetazolamide
Hemodialysis
Hyperparathyroidism
EFFECTS
Irritability
Confusion
Metabolic encephalopathy
Coma
Muscle weakness
Respiratory failure
Failure to wean from ventilator
Dysphagia
Ileus
cardiac arrhythmias and cardiomyopathy.
ODC shift to left
TREATMENT
Asymptomatic mild-to-moderate hypophosphatemia (1-2.5 mg/dL) can be treated with oral phosphate supplementation if the gastrointestinal tract is intact.
Symptomatic or severe hypophosphatemia (< 1.0 mg/dL) should be treated with intravenous phosphate.
Oral supplementation : 2.5 to 3.5 g (80 to 110 mmol) per day, divided over two to three doses.
Intravenous:
The required dose of initial intravenous phosphate may vary from 2.5 to 19.8 mg/kg.
Typically, 2-5 mg/kg of inorganic phosphate dissolved in 0.45% saline is given over 6-12 hours and repeated as needed.
Rapid or large infusions are dangerous : Large intravenous doses of phosphate may result in hyperphosphatemia, hypomagnesemia, hypocalcemia, and hypotension.
Hyperkalemia is prevented by using sodium phosphate instead of potassium phosphate in patients with potassium levels >4 mmol/L.
Do not mix with Calcium or Magnesium
Daily Phosphate level monitoring should be done
〰NEW INSIGHTS〰
FGF23 recently identified as a physiological regulator of phosphate and vitamin D metabolism
FGF23 plays a central role in the pathogenesis of altered mineral metabolism and secondary hyperparathyroidism in CKD patients and post-transplant hypophosphatemia in kidney transplant recipients.
FGF23 can be used not only as a biomarker for assessing phosphate retention but also as a predictor of mortality and future development of re- fractory hyperparathyroidism.
ANTICOAGULANTS OF CHOICE IN VARIOUS LABORATORY TESTS
ESR WESTERGREN’S
COAGULATION STUDIES –> SODIUM CITRATE
ESR WINTROBE’S
PERIPHERAL SMEAR–> EDTA
Hb , PCV –> DOUBLE OXALATE
OSMOTIC FRAGILITY –> HEPARIN
BLOOD SUGAR–> SODIUM FLURIDE + OXALATE
The Lay Medical Man 