- Aerosols are small particles of liquids or solids suspended in a carrying gas
- Medical aerosols can be produced by a nebulizer
- The therapeutic efficacy of the aerosol is dependent on the liquid or solid’s ability to remain in suspension and the depth reached by the aerosol on inhalation, and is dependent on its stability. These are both determined by the particle size.
- For liquid medication to enter the alveoli the droplets must be smaller than the diameter of the terminal bronchioles and fall within the size range of 0.005 µm to 50 µm in diameter.
- For droplet sizes below 5 µm, gravity exerts a negligible effect.
- Particles or droplets in the range 5 to 10 µm tend to deposit in the upper airways, with material below 5 µm penetrating further into the lungs.
- Below 3 µm, the droplets enter the alveoli and become therapeutically beneficial.
- Droplets below 1 µm are ideal; but if significantly smaller than this, the particles will be exhaled without having a therapeutic effect.
- The temperature for an aerosol generated by a nebulizer must not exceed 37°C and the process must not alter the structure of the medication being carried.
- This is the essential difference between vaporizers that generate a vapour and nebulizers that produce liquid droplets.
- Jet or gas driven nebulizer (atomizers)
- A high flow of gas is driven over a capillary tube that is immersed into the fluid to be nebulized. The high pressure air driven through the small orifice, generates negative pressure as a result of the Venturi effect. These nebulizers are simple and low cost, but small variations in gas flow rate can result in inconsistent delivery of aerosol to the patient.
- Ultrasound driven nebulizer
- The ultrasound nebulizer incorporates a ceramic piezoelectric transducer that changes electrical energy into mechanical energy (pressure oscillations). The transducer sits at the bottom of the chamber and vibrates at a frequency of 1.5 MHz. The vibrations are transmitted through the water. The diaphragm is in contact with the solution to be nebulized and violently shakes the solution into particles. At low frequencies, larger particles are produced, but at higher frequencies, a fine mist is generated
- Ultrasonic nebulizers tend to produce a more consistent particle size than jet nebulizers and, as a result, produce a much greater deposition into the lungs.
- But long-term use of ultrasonic nebulization might inadvertently affect surface tension stability in the alveoli
Category Archives: Drugs and Pharmacology
Morphine and Hydromorphone
- Morphine is metabolised via hepatic system and excreted by renal system
- It can get accumulated in hepatic/renal dysfunction and obesity
- Morphine has 2 metabolites:
- Morphine 6 glucoronide- Active metabolite: responsible for analgesia and sedation
- Morphine 3 glucoronide: Can cause seizures
- Morphine has histamine releasing property
- Hydromorphone is more potent than morphine
- Hydromorphone doesnt have active metabolites
- Hydromorphone lacks histamine release
Protamine
DOXAPRAM
VOLTAGE & LIGAND GATED ION CHANNELS
THE SPECIFIC MECHANISMS OF ACTION OF #MANNITOL IN VARIOUS CLINICAL SITUATIONS
Mannitol is a monosaccharide available as 10% & 20% solutions
DURING NEUROSURGERY/ IN NEUROCRITICAL CARE:
✔️Mannitol is freely filtered in the glomerulus but won’t get reabsorbed in the tubules; so it will drive water from the interstitium which gets eliminated as urine. Hence acts as an osmotic diuretic
✔️When blood brain barrier is intact, the osmotic gradient created by mannitol will move water from the cerebral extravascular compartment to the intravascular space, reducing ICP. If blood brain barrier is not intact, it will worsen cerebral edema.
✔️The expansion of the plasma volume caused by mannitol will reduce the viscosity and improve cerebrovascular microcirculation and oxygenation. The increase in cardiac output can also cause an increase in regional blood flow which will cause a compensatory cerebrovascular vasoconstriction in areas where autoregulation is intact.
IN CRUSH INJURY / MYOGLOBINURIA
✔️Will release renal prostaglandins, which will cause renal vasodilation and increase tubular urine flow causing a solute washout and avoidance of tubular obstruction #TheLayMedicalMan
MECHANISM BEHIND ADVERSE EFFECTS
✔️The initial increase in plasma volume as a result of drawing of water into the vascular component and the resultant increase in cardiac output can precipitate heart failure in cardiac patients
✔️The osmotic diuresis can cause hypernatremia [increases urinary losses of both sodium and electrolyte-free water] , metabolic acidosis and hyperosmolarity. It has been advised that therapy should be monitored and titrated so that osmolarity doesn’t go up beyond 300 mOsm/L
✔️The rise in the plasma potassium concentration following hypertonic mannitol is due to the movement of potassium out of the cells into the extracellular fluid as the rise in cell potassium concentration induced by water loss favors passive potassium exit through potassium channels in the cell membrane
✔️Though it has been used for renal protection, the reduction in renal perfusion resulting from hypovolemia caused by diuresis can adversely affect renal function; so should be avoided in patients with renal dysfunction
#Neuroanesthesia , #Anesthesia , #Neurology , #CriticalCare
WHAT IS POYNTING EFFECT ❓
ICTAL BRADYCARDIA AND ASYSTOLE : AN ENTITY ALL ANESTHESIOLOGISTS SHOULD KEEP IN MIND WHEN SEEING BRADYCARDIA IN A PATIENT WITH EPILEPSY
📌Ictal bradycardia/asystole is a poorly recognised cause of collapse late in the course of a typical complex partial seizure
📌It is important to identify ictal bradycardia as a potential harbinger of lethal rhythms, such as asystole, as this may be one important mechanism leading to sudden unexpected death in epilepsy (SUDEP)
📌Tachycardia is the most common rhythm abnormality occurring in 64–100% of temporal lobe seizures. Ictal bradycardia has been reported in less than 6% of patients with complex partial seizures
📌The ictal bradycardia syndrome occurs in mostly in patients with temporal lobe seizures.
📌It is believed that abnormal neuronal activity during a seizure can affect central autonomic regulatory centres in the brain leading to cardiac rhythm changes.
📌Ictal bradycardia/asystole may be unrecognised until documented during video-electroencephalograph (video EEG)–electrocardiogram (ECG) monitoring in those with refractory epilepsy, often in the context of pre-surgical evaluation
📌Other rhythm abnormalities which can occur are change in heart rate variability, ictal tachycardias and atrioventricular (AV) block
📌If sufficiently severe, the ictal-induced bradyarrhythmia temporarily impairs both cerebral perfusion and cortical function; the result has the dual effect of terminating the seizure, while at the same time triggering syncope with consequent loss of consciousness and postural tone. In essence, a complex partial seizure patient may manifest both seizure and syncope features during the same episode.
📌There are currently no guidelines on who should undergo further cardiovascular investigations ; dual chamber pacemaker implantation has been suggested as a treatment in the long term, for epilepsy patients who manifest this syndrome and suffer repeated falls; but there is not much mention in literature both about diagnosis and about pharmacological and non pharmacological interventions to counter such episodes when presenting as an emergency situation in the perioperative scenario , especially when the patient is under anesthesia.
#Neurology , #NeuroCriticalCare , #Anesthesia , #LayMedicalMan , #CriticalCare , #Epilepsy , #Cardiology , #CardiacAnesthesia
Reference: Ictal bradycardia and atrioventricular block: a cardiac manifestation of epilepsy; Salman S. Allana Hanna N. Ahmed Keval Shah Annie F. Kelly, Oxford Medical Case Reports, British Journal of Cardiology : Ictal Bradycardia and Asystole Associated with Intractable Epilepsy: A Case Series Elijah Chaila, Jaspreet Bhangu, Sandya Tirupathi, Norman Delanty; Ictal Asystole-Life-Threatening Vagal Storm or a Benign Seizure Self-Termination Mechanism? David G. Benditt, Gert van Dijk, Roland D. Thijs (Editorial:Circulation )
#EPINEPHRINE ( #Adrenaline) : Pharmacological Highlights
🔻Epinephrine is an agonist of alpha 1, β1 , and β2 adrenoceptors. An intravenous infusion of epinephrine produces an increase in mean arterial pressure (MAP) characterized by selectively enhanced systolic pressure with no change in diastolic pressure.
🔻Epinephrine exerts positive chronotropic and inotropic actions by stimulation of β1 adrenoceptors
🔻Epinephrine also increases the rate of myocardial relaxation and enhances early LV filling, thereby improving diastolic function. These combined effects result in a dramatic increase in cardiac output.
🔻Epinephrine (0.01–0.03 ug kg –1 min –1 ) has been shown to produce similar hemodynamic effects with less pronounced tachycardia than dobutamine (2.5–5.0 ug kg–1 min–1 ) in patients after coronary artery bypass graft (CABG) surgery
🔻Predictable increase in cardiac output, favours the use of epinephrine as the primary inotropic drug for the management of LV dysfunction after cardiopulmonary bypass
🔻Epinephrine causes direct positive dromotropic effects ( leading to increase in conduction velocity and reduction of the refractory period of the AV node, His bundle, Purkinje fibers, and ventricular muscle)
🔻This may contribute to detrimental increases in ventricular rate in patients with atrial flutter or fibrillation and the occurrence of ventricular arrhythmias
🔻The overall effect of epinephrine on blood flow to a specific organ depends on the relative balance of alpha 1 and β2 adrenoceptors located in the vasculature.
🔻β2 -Adrenoceptors are sensitive to lower doses of epinephrine and, as a result, peripheral vasodilation and modest reductions in arterial pressure are observed with such doses
🔻In contrast, the effects of epinephrine on alpha 1 -adrenoceptors predominate at greater doses with marked increases in systemic vascular resistance and arterial pressure.
🔻The intense vasoconstriction produced by high doses of epinephrine may adversely impede LV ejection by increasing after load after cardiopulmonary bypass. Thus, greater doses of epinephrine may be used in combination with arterial vasodilators such as sodium nitroprusside to optimize contractile performance in such situations .
🔻Adrenaline via alpha 1 receptors also mediates (1) venoconstriction & enhanced venous return (2) Pulmonary vasoconstriction and increases in pulmonary arterial pressures.
🔻 Pre-existing β-blockade by nonselective β-blocker propranolol abolishes the decrease in systemic vascular resistance from epinephrine-induced stimulation of β2 adrenoceptors and potentiates peripheral vasoconstriction mediated by unopposed alpha 1 adrenoceptors.
🔻The positive inotropic and chronotropic effects of epinephrine are also attenuated in the presence of pre-existing β-blockade and greater doses of epinephrine are required to overcome this competitive blockade
🔻Complete pharmacologic blockade of β1 and β2 adrenoceptors may theoretically make the hemodynamic effects of epinephrine indistinguishable from those of the pure alpha 1 adrenoceptor agonist phenylephrine.
#NorAdrenaline , #CriticalCare , #vasopressors , #TheLayMedicalMan , #IntensiveCare , #Pharmacology, #anesthesia , #anaesthesia, #drugs
(Reference: Paul S. Pagel and David C. Warltier, Essential drugs in anesthesia practice Positive inotropic drugs, Anesthetic Pharmacology, 2nd edition)
JNC 8 GUIDELINES FOR MANAGEMENT OF SYSTEMIC HYPERTENSION
(1)📌In the general population aged 60 years or more , initiate pharmacologic treatment to lower blood pressure (BP) at systolic blood pressure (SBP) ≥150 mm Hg or diastolic blood pressure (DBP) ≥90 mm Hg and treat to a goal SBP <150 mm Hg and goal DBP <90 mm Hg
(2)📌In the general population aged ≥60 years, if pharmacologic treatment for high BP results in lower achieved SBP (eg, <140 mm Hg) and treatment is well tolerated and without adverse effects on health or quality of life, treatment does not need to be adjusted.
(3)📌In the general population <60 years, initiate pharmacologic treatment
(a) to lower BP at DBP ≥90mmHg and treat to a goal DBP <90mmHg.
(b) to lower BP at SBP ≥140 mm Hg and treat to a goal SBP <140 mm Hg.
(4)📌In the population aged ≥18 years with (i) diabetes & (ii) chronic kidney disease (CKD), initiate pharmacologic treatment to lower BP at SBP ≥140 mmHg or DBP ≥90 mmHg and treat to goal SBP <140mmHg and goal DBP <90mmHg.
(5)📌In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor
(ACEI), or angiotensin receptor blocker (ARB).
(6)📌In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB.
(7)📌In the population aged 18 years with CKD, initial (or add-on) antihypertensive treatment should include an ACEI or ARB to improve kidney outcomes. This applies to all CKD patients with hypertension regardless of race
or diabetes status.
(8)📌If goal BP is not reached within a month of treatment, increase the dose of the initial drug or add a second drug from one of the classes : thiazide-type diuretic, CCB,ACEI, or ARB. The clinician should continue to assess BP and adjust the treatment regimen until goal BP is reached.
(9)📌If goal BP cannot be reached with 2 drugs, add and titrate a third drug from the list mentioned above (). Do not use an ACEI and an ARB together in the same patient.
(10)📌If goal BP cannot be reached using only the drugs mentioned above, because of a contraindication or the need to use more than 3 drugs to reach goal BP, antihypertensive drugs from other classes can be used.
#hypertension , #medicine , #TheLayMedicalMan , #jnc8 , #HTN , #anesthesia , #pharmacology , #BloodPressure ,#BP
The Lay Medical Man 