Author Archives: Dr Unnikrishnan Prathapadas

THE BASICS OF RESPIRATORY PHYSIOLOGY

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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:

  1. 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
  2. Ventilation and perfusion are matched
  3. 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

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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

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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?

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MNEMO>

Aorta is the vessel, which ‘TURNs back’

Answer: Coarctation of Aorta, Aortic Valvular Disease!!

REFINE YOUR IMPRESSION OF 📕PaO2 Vs 📗SaO2 Vs 📘CaO2

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⭕️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).

 

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Labetalol Pharmacology

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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

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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

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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

POSTOPERATIVE AGITATION / EMERGENCE DELIRIUM IN CHILDREN AFTER SEVOFLURANE ANAESTHESIA

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Incidence up to more than 40%

Might be occurring together with EEG-changes

Methods usually tried to reduce the incidence: addition of nitrous oxide, premedication with benzodiazepines, early extubation, switching to other inhaled anaesthetics

Propofol maintenance after sevoflurane induction seems to be the best alternative.

A recent study also indicates that a switch to desflurane for maintenance after sevoflurane inhalation induction reduces the incidence of emergence agitation by 50 %

A paranoid delusion is said to be a common feature of this state of agitation.

Information about this phenomenon should be explained to the parents before the procedure.

D for DANTROLENE

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Dantrolene inhibits calcium release via RyR1 antagonism and impairs calcium-dependent muscle contraction.

This rapidly halts the increases in metabolism and secondarily results in a return to normal levels of catecholamines and potassium.

Dose is 2 mg/kg; repeat every 5 minutes until vital signs normalise, to a total dosage of 10 mg/kg if needed.

Dantrolene takes ~ 6 minutes to have any effect

The solution is prepared by mixing 20 mg of dantrolene with 3 g of mannitol in 60 ml of sterile water. Reconstitute each 20 mg vial with 60 ml sterile water. The powder for reconstitution contains mannitol and Sodium hydroxide. Use within 6 hours.

Since dantrolene is relatively insoluble, preparation is tedious and time consuming, and its preparation should not be the responsibility of the primary anesthesiologist involved in the patient’s management. (May occupy several nurses)

All patients who develop MH, require at least 24 hours of posttreatment management in a critical-care setting as there is chance of reappearance of symptoms ( known as recrudescence )

In the ICU, continue @1mg/kg q6h for 24 hours
May be given enterally if GIT function is normal (price ~ 1000 x less)

The actions of dantrolene include:

inhibition of release of Ca ++ from the SR, without affecting re-uptake
? antagonises the effects of Ca ++ at the actin/myosin – troponin/tropomyosin level
muscular weakness, which may potentiate NMJ blockade ~ 5-15 mg/kg produces significant muscular relaxation
there is no effect on NMJ transmission
up to 15 mg/kg there is no significant effect on the CVS
up to 30 mg/kg there is no significant effect on respiration

#dantrolene , #MalignantHyperthermia, #mh ,#anaesthesia