WHEN VENTILATOR GIVEs ALARM & SHOWS ‘PATIENT-DEMAND IS HIGH’ : Troubleshooting the Ventilator

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Check for causes:

Increased airway resistance- if so give bronchodilators

Anxiety–> increased RR + muscle tension–> increased airway resistance –> increased demand: Optimise sedation

Check for leaks in circuit and correct

If flow rate seems too low: Set higher inspiratory flow rate or reduce inspiratory time especially if patient is showing tachypnea

If Tidal volume or RR set too low: Increase it

Double triggering or breath stacking can happen if inspiratory time set is lower compared to that of the patient and ventilatory demand is high: Try increasing the inspiratory time or change to pressure control modes

NB:

Peak Inspiratory Pressure high with normal Plateau Pressure = it’s Increased airway resistance

Both (a)Peak Inspiratory Pressure and (b)Plateau Pressure are high and (a)-(b) is normal= it’s reduced compliance or auto peep

#CriticalCare , #MechanicalVentilation ,#VentilationBasics , #Ventilation , #anesthesia , #anesthesiologist , #ICUnurse , #ICUdoctor , #ICU

MECHANICAL VENTILATION FACTS

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LOW FLOW Anesthesia

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Low flow anesthesia allows for economy of volatile anesthetics, makes possible heating and humidification of gases and reduces environmental pollution

Sodalime contains 94% Calcium hydroxide, 5% Sodium hydroxide and also Potassium hydroxide, Silica and dying agent

CO2 + 2NaOH –> Na2CO3 + water + heat

Na2CO3 + Ca(OH)2 –> 2NaOH + CaCO3

..this sequence gets back Sodium hydroxide

1 Kg of Sodalime can absorb >120 L of CO2

Carbon monoxide which is a byproduct of protein metabolism can accumulate in the system, but levels are <4%

If there is intoxication by alcohol or poisoning by Carbon monoxide or severe diabetic ketosis, alcohol or CO or acetone from the expired gases, will recirculate and accumulate inside the system; so low flow anesthesia is contraindicated in such states

Prolonged anesthesia with sevoflurane may generate Compound A inside the system, which can cause acute tubular necrosis in rats at concentrations around 250 ppm, a dose that is nearly 200 times seen in clinical practice. So any proteinuria, glycosuria or enzymuria which does develop in such a context has not been shown to have any clinical significance, even in patients with pre-existing renal disease

Reference: Al-Shaikh B, Stacey S. Essentials of Anaesthetic Equipment, 2nd edn. Edinburgh: Churchill Livingstone, 2002; pp. 74–9 . Nunn G. Low-flow anaesthesia. Contin Educ Anaesth Crit Care Pain 2008; 8: 1–4.

POSTOPERATIVE VISUAL LOSS

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Corneal abrasion is the most common ocular complication after general anesthesia

Ischemic Optic neuropathy (ION) and Central Retinal Artery Occlusion (CRAO) are the commonest causes for postoperative visual loss

ISCHEMIC OPTIC NEUROPATHY (ION)

More common among the two

Most often seen after prolonged surgery in prone position

Venous congestion–> Raised Intra Ocular Pressure (IOP) due to Raised Intra Orbital Pressure –> Intra Orbital ‘Compartment Syndrome’

Hypotension, Diabetes, Vascular disease, Smoking etc also may be important in the etiopathogenesis

Treatment:

Reduce optic nerve edema as it passes through posterior scleral foramen with steroids and mannitol

Optimal oxygen delivery by ensuring normal blood pressure and hematocrit

Clear all obstruction to venous drainage

Chance of visual recovery is less

CENTRAL RETINAL ARTERY OCCLUSION (CRAO)

External pressure on eye and embolism are risk factors

An echocardiogram and carotid ultrasound may help us to find an embolic source

Reference: White E, David DB. Care of the eye during anaesthesia and intensive care. Anaesth Intens Care Med. 2007; 8(9): 383–386.

SUGAMMADEX & DRUG INTERACTIONS

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Sugammadex acts by forming a complex with steroidal Neuro Muscular Blocking Agents such as rocuronium and vecuronium and reduces their concentrations in the neuromuscular junction.

Because of its inert structure, direct drug interactions are rarely expected with sugammadex. Two types of drug interactions may occur with sugammadex by displacement or capturing.

Drugs interacting with sugammadex by displacement : toremifene, fusidic acid, and flucloxacillin, could potentially affect the efficacy of sugammadex due to rocuronium
or vecuronium being displaced from sugammadex.

Capturing interactions may occur if sugammadex binds with other drugs (i.e., hormonal contraceptives), and reduces their free plasma concentration. In addition, sugammadex might have decreased efficacy for rocuronium or vecuronium due to it binding with another drug.

Cyclodextrins have been reported to form inclusion complexes with other compounds.

In an in vitro experimental model of functionally innervated human muscle cells Rezonja et al. found that dexamethasone led to a dose-dependent inhibition of sugammadex reversal; but Ersel Gulec et al, who investigated the clinical relevance of the interaction between dexamethasone and sugammadex in humans failed to demonstrate any inhibitory effect of dexamethasone (0.5 mg/kg) on the reversal time of sugammadex in children.

N.B.(DO YOU KNOW?): It is clearly demonstrated that dexamethasone attenuates rocuronium-induced neuromuscular blockade when administered 2 to 3 hours before the induction of anesthesia; but not when dexamethasone is given at induction

Reference: The Effect of Intravenous Dexamethasone on Sugammadex Reversal Time in Children Undergoing Adenotonsillectomy; Ersel Gulec, Ebru Biricik, Mediha Turktan, Zehra Hatipoglu and Hakki Unlugenc, April 2016 • Volume 122 • Number 4, anesthesia-analgesia

ANTIDEPRESSANTS; AS ANALGESIC Vs AS ANTIDEPRESSANT

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The tricyclic antidepressants prevent the reuptake of monoamines, including serotonin and noradrenaline, as both pathways are important in the pain propagation. So the mixed reuptake drugs work better than more selective drugs like SSRIs

But serotonin-noradrenaline reuptake inhibitor antidepressants (SNRIs), for example, venlafaxine & duloxetine and the atypical antidepressant group, such as bupropion and mirtazapine are also effective for some chronic pain conditions and are increasingly used because of their improved tolerability

The superiority of tricyclics, particularly clomipramine and amitriptyline, in the management of pain may also be explained by their additional action on sodium channels blockade ( which is an action that SNRIs do not exhibit.)

The dose of amitriptyline to treat pain is much lower when compared to that needed to treat depression

The analgesic action has a faster onset, whereas antidepressant action takes weeks to start

The sedative action of tricyclic antidepressants are helpful in treating the sleep disturbances associated with neuropathic syndromes. Nortriptyline is less sedative than amitriptyline.

#antidepressants , #analgesics , #PainManagement , #ChronicPain

Reference: Medscape, Pharmacogenetics and Analgesic Effects of Antidepressants in Chronic Pain Management, Frédérique Rodieux; Valérie Piguet; Patricia Berney; Jules Desmeules; Marie Besson, Personalized Medicine. 2015;12(2):163-175.
Ryder S A, Stannard C F. Treatment of chronic pain: antidepressant, antiepileptic and antiarrhythmic drugs. Contin Educ Anaesth Crit Care Pain 2005; 5: 18–20 .

A TRAVELOGUE: The long journey of Insulin

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Insulin is produced by beta cells of islets of Langerhans.

It is produced from the pro hormone, ‘preproinsulin’ in endoplasmic reticulum. A portion of the structure is cleaved off and the remaining portion is folded with the help of C-peptide to form ‘proinsulin’

The C-peptide portion is then removed to form Insulin

This active Insulin is transported via Golgi apparatus to cytoplasmic granules for exocytosis into plasma

Insulin then binds with its receptor on Insulin sensitive cells

Insulin receptor is a tetramer consisting of 2 alpha & 2 beta units.

Insulin binds to the alpha unit on the cell membrane, while the beta unit, which spans the cell membrane activates tyrosine kinase and the second messenger system

This activates cytoplasmic vesicles containing transport molecules

The vesicles fuse with the cell membrane to incorporate the transport molecules into the cell membrane, which facilitate the transport of glucose into the cell.

MNEMO> MECHANISM OF ACTION: INSULIN Vs GLUCAGON

Insulin binding to the receptor activates an intracellular second-messenger system via tyrosine kinase.
Glucagon binding to its receptor activates a G-protein second-messenger system via adenylyl cyclase.

“Insulin is TricKy”
“Glucagon is ACcurate”

A FEW CLUES IN INTERPRETING AN ISOLATED PROLONGATION OF ACTIVATED PARTIAL THROMBOPLASTIN TIME (aPTT)

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aPTT tests the intrinsic and common pathways of coagulation

Though it is included commonly as a part of coagulation profile assessment, it’s primary uses are to detect coagulation factor deficiency and titration of heparin therapy

An isolated elevation of aPTT may indicate

deficiency of Factor VIII or IX or XI or XII

acquired clotting factor inhibitors

presence of Lupus anticoagulant

N.B.:- Factor VIII deficiency is Haemophilia A, Factor IX deficiency is Haemophilia B and Factor XI deficiency is Haemophilia C

If factor levels are >30% of normal, aPTT may remain normal, for e.g. in mild von Willebrand disease [raised aPTT + prolonged Bleeding Time (BT)], in mild hemophilia etc

Reference: Martlew V. Peri-operative management of patients with coagulation disorders. Br J Anaesth. 2000; 85(3): 446–455.

HOMOCYSTINURIA : Anesthesia IMPLICATIONS

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There is increased levels of homocystine and methionine in blood and urine due to the deficiency of Cystathionine B synthetase which catalyses the conversion of homocystine and serine into cystathionine

Raised cystine levels reduce the resistance of endothelium against thrombosis, reduces the activity of the vasodilator nitric oxide (NO) and increase platelet aggregation. So there is high incidence of thromboembolism. We have to ensure good hydration, good cardiac output,early mobilisation and should provide mechanical +/- pharmacological thromboprophylaxis. Many patients will be on anticoagulation. If untreated 50% of patients will have thromboembolic complications and the mortality is about 20% before the age of 30 years. So both modification of the dosing of anticoagulants ( especially if regional anesthesia is planned) if patient is receiving them and providing prophylaxis against DVT are important elements of perioperative care. The incidence of thrombotic complications are more in pregnant patients.

Blood viscosity and platelet adhesiveness can be reduced by dextran, and the prior administration of pyridoxine

Reduced cystine results in weak collagen and fragmentation of elastic tissue of large arteries. There is high incidence of vascular diseases like Cerebrovascular diseases, Coronary Artery Disease, Peripheral Vascular Diseases

Patients may have increased insulin levels resulting in hypoglycemia. Dextrose infusion will prevent hypoglycaemia.

Acute psychiatritc symptoms, delirium etc have been reported and the altered availability of homocysteine, methionine and cystiene which are having glutamate agonist properties, has been postulated as a factor which promotes this.

Regional anaesthesia has certain theoretical disadvantages. Penetration of a large epidural blood vessel might initiate thrombosis, as may the accompanying venous stasis of the lower limbs.

Reference: ANAESTHESIA DATABOOK, A Perioperative and Peripartum Manual, 3RD EDITION
Rosemary Mason

A FEW FACTS ABOUT COAGULATION FUNCTION, IT’S MONITORING & Regional Anesthesia IN OBSTETRIC PATIENTS

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During routine epidural or spinal anaesthesia, accidental puncture of epidural veins occurs in 1–18% of patients

The incidence of hematoma after epidural techniques is estimated to be in the order of 1:150,000 after epidural placement and 1:220,000 after spinal injection in the general population

removal of epidural catheters posed an equal risk to insertion ( Van- dermeulen et al)

Surgery on spinal haematoma should ideally be performed within 8–12 h of the identification of symptoms in order to improve the chances of recovery.

The overall risk of death in those having general anaesthesia for caesarean section was quoted in 2007 as being just over 1:25,000.

The levels of factors VII, VIII and fibrinogen increase and those of anticoagulation factors decrease, causing augmented coagulation and decreased fibrinolysis in pregnancy.

There is no evidence to support routine full blood count (FBC) or coagulation tests in women before the performance of a regional block in those who have had

normal FBC results

no bleeding history

no signs or symptoms of liver disease

no signs or symptoms of pre-eclampsia, abruption or clinical signs of disseminated intravascular coagulation

no recent anticoagulant treatment.

In women with known thrombocytopaenia, a Full Blood Count (FBC) should be checked within 24 h of a regional procedure.

In women with mild to moderate pre-eclampsia, the course of the disease can be unpredictable and so FBC be checked within 6 h. In addition, coagulation tests should be performed if platelets are <100000/mcL or if there is abnormal liver function.

In severe disease, FBC and clotting should be checked immediately before a procedure, as platelet levels in particular can decline rapidly.

Women with pregnancy-induced hypertension alone do not require an FBC before a regional procedure

Activated partial thromboplastin time ratio (APTTR) and international normalised ratio (INR) are slightly decreased in late pregnancy.

In a patient who receives LMWH, if he/she is simultaneously taking NSAID+Aspirin, there is an increased risk if last dose of LMWH is between 12-24 hours; it further increases if last dose is <12 hours

In patients with pre-eclampsia and platelet count between 75000-100000/mcL, there is an increased risk even if coagulation tests are normal; but it increases further if the counts has not been stable (=decreasing platelet count)

#obstetrics , #anesthesia , #coagulation , #anaesthesia

Reference: Abnormalities of Coagulation and Obstetric Anaesthesia, Hilary Swales, AAGBI Core Topics in Anaesthesia 2015