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Metabolic causes
Structural causes
Drug related causes
Infections
Endocrine causes
Last but not least – Psychiatric causes
Updated 11/18/09
1/25/09 Some notes on Neuromuscular-blocking drugs: -most taken from Wikipedia These drugs fall into two groups: Depolarizing blocking agents: (succinylcholine) These agents act by depolarizing the plasma membrane (cell membrane) of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh. Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. However, these agents are more resistant to degradation by acetylcholinesterase (AChE), the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers. This differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle. There are two phases to the depolarizing block. During phase I (depolarizing phase), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually, after sufficient depolarization has occurred, phase II (desensitizing phase) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. At this point, full neuromuscular block has been achieved Non-depolarizing blocking agents: (e.g. Vecuronium )These agents constitute the majority of the clinically-relevant neuromuscular blockers. They act by blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.
1/25/09
Some notes on Neuromuscular-blocking drugs: -most taken from Wikipedia
These drugs fall into two groups:
Class: Depolarizing Neuromuscular Blocker Description: Succinylcholine is a short acting, depolarizing skeletal muscle relaxant used to facilitate endotracheal intubation. Mechanism of Action: Like acetylcholine, Succinylcholine combines with cholinergic receptors in the motor nerves to cause depolarization. Neuromuscular transmission is thus inhibited, which renders the muscles unable to be stimulated by acetylcholine. Complete paralysis is obtained within 60 to 90 seconds, and persists for approximately 4 to 5 minutes. Effects then begin to fade, and a return to normal is seen within 6 minutes. Muscle relaxation begins in the eyelids and the jaw, and then progresses to the limbs, abdomen, diaphragm, and intercostals. Succinylcholine has no effect on consciousness. Indications: Succinylcholine is used to achieve temporary paralysis when endotracheal intubation is indicated, and muscle tone or seizure activity prevents it. Contraindications: Known hypersensitivity, penetrating eye injuries, and narrow-angle-glaucoma. Precautions: Succinylcholine should not be administered unless personnel skilled in endotracheal intubation are present and ready to perform the procedure. Oxygen and emergency resuscitative drugs should be readily available. Cardiac arrest and ventricular arrhythmias have been reported when Succinylcholine was administered to patients with severe burns and severe crush injuries. Side Effects: Succinylcholine can cause wheezing, respiratory depression, apnea, aspiration, arrhythmias, bradycardia, sinus arrest, hypertension, hypotension, increased intraocular pressure, increased intracranial pressure. Interactions: Lidocaine, Procainamide, beta-blockers, magnesium sulfate, and other neuromuscular blockers enhance the effects of Succinylcholine. Dosing: 1.5mg/kg IVP
Class:
Depolarizing Neuromuscular Blocker
Description:
Succinylcholine is a short acting, depolarizing skeletal muscle relaxant used to facilitate endotracheal intubation.
Mechanism of Action:
Like acetylcholine, Succinylcholine combines with cholinergic receptors in the motor nerves to cause depolarization. Neuromuscular transmission is thus inhibited, which renders the muscles unable to be stimulated by acetylcholine. Complete paralysis is obtained within 60 to 90 seconds, and persists for approximately 4 to 5 minutes. Effects then begin to fade, and a return to normal is seen within 6 minutes. Muscle relaxation begins in the eyelids and the jaw, and then progresses to the limbs, abdomen, diaphragm, and intercostals. Succinylcholine has no effect on consciousness.
Indications:
Succinylcholine is used to achieve temporary paralysis when endotracheal intubation is indicated, and muscle tone or seizure activity prevents it.
Contraindications:
Known hypersensitivity, penetrating eye injuries, and narrow-angle-glaucoma.
Precautions:
Succinylcholine should not be administered unless personnel skilled in endotracheal intubation are present and ready to perform the procedure. Oxygen and emergency resuscitative drugs should be readily available. Cardiac arrest and ventricular arrhythmias have been reported when Succinylcholine was administered to patients with severe burns and severe crush injuries.
Side Effects:
Succinylcholine can cause wheezing, respiratory depression, apnea, aspiration, arrhythmias, bradycardia, sinus arrest, hypertension, hypotension, increased intraocular pressure, increased intracranial pressure.
Interactions:
Lidocaine, Procainamide, beta-blockers, magnesium sulfate, and other neuromuscular blockers enhance the effects of Succinylcholine.
Dosing: 1.5mg/kg IVP
Class: General anesthetic and adjunct to general anesthesia Description: Etomidate is a short-acting, intravenously administered sedative hypnotic. Etomidate has a rapid onset of action and recovery. It has minimal cardiac and respiratory-depressive effects and causes no histamine release, so it is useful in patients with compromised cardiopulmonary function. Mechanism of Action: Etomidate appears to facilitate GABAminergic neurotransmission by increasing the number of available GABA receptors, possibly by displacing endogenous inhibitors of GABA binding. Etomidate produces clinical responses such as hypnosis, elevations in arterial carbon dioxide tension, reduced cortisol plasma levels, and a transient 20—30% decrease in cerebral blood flow. Its effects are at least partially due to depression of the brainstem reticular formation. Indications: Induction of general anesthesia. Contraindications: Use with caution in the elderly and in patients with hepatic disease because they are more likely to develop etomidate-related adverse reactions. Precautions: Use with caution during lactation. Side Effects: Skeletal muscle: Myoclonic skeletal muscle movements, tonic movements. Respiratory: Apnea of short duration, hyperventilation or hypoventilation, laryngospasm. CV: Either hypertension or hypotension; tachycardia or bradycardia; arrhythmias. GI: Postoperative N&V. Miscellaneous: Eye movements, averting movements, hiccoughs, snoring. Interactions: Etomidate potentiates the effects of CNS depressants such as ethanol, general anesthetics, local anesthetics, antidepressants, H1-blockers, opiate agonists, skeletal muscle relaxants, phenothiazines, barbiturates, and benzodiazepines. Concurrent use of antihypertensive agents and etomidate can result in hypotension. This is particularly true if any of the following agents are used with etomidate: calcium-channel blockers, diazoxide, mecamylamine. Dosing: 0.3mg/kg IVP
General anesthetic and adjunct to general anesthesia
Etomidate is a short-acting, intravenously administered sedative hypnotic. Etomidate has a rapid onset of action and recovery. It has minimal cardiac and respiratory-depressive effects and causes no histamine release, so it is useful in patients with compromised cardiopulmonary function.
Etomidate appears to facilitate GABAminergic neurotransmission by increasing the number of available GABA receptors, possibly by displacing endogenous inhibitors of GABA binding. Etomidate produces clinical responses such as hypnosis, elevations in arterial carbon dioxide tension, reduced cortisol plasma levels, and a transient 20—30% decrease in cerebral blood flow. Its effects are at least partially due to depression of the brainstem reticular formation.
Induction of general anesthesia.
Use with caution in the elderly and in patients with hepatic disease because they are more likely to develop etomidate-related adverse reactions.
Use with caution during lactation.
Skeletal muscle: Myoclonic skeletal muscle movements, tonic movements. Respiratory: Apnea of short duration, hyperventilation or hypoventilation, laryngospasm. CV: Either hypertension or hypotension; tachycardia or bradycardia; arrhythmias. GI: Postoperative N&V. Miscellaneous: Eye movements, averting movements, hiccoughs, snoring.
Etomidate potentiates the effects of CNS depressants such as ethanol, general anesthetics, local anesthetics, antidepressants, H1-blockers, opiate agonists, skeletal muscle relaxants, phenothiazines, barbiturates, and benzodiazepines. Concurrent use of antihypertensive agents and etomidate can result in hypotension. This is particularly true if any of the following agents are used with etomidate: calcium-channel blockers, diazoxide, mecamylamine.
Dosing: 0.3mg/kg IVP
(Versed) Class: Sedative and Hypnotic Description: Midazolam is a benzodiazepine with strong hypnotic and amnestic properties. Mechanism of Action: Midazolam is a potent but short-acting benzodiazepine used as a sedative and hypnotic. It is three to four times more potent than Diazepam. Its onset of action is approximately 1.5 minutes when administered IV. Midazolam has impressive amnestic properties, and like other benzodiazepines, it has no effect on pain. Indications: Midazolam is used as a premedication before cardioversion and other painful procedures. Contraindications: Known hypersensitivity, narrow angle glaucoma, shock, depressed vital signs, and alcoholic coma. Precautions: Emergency resuscitative equipment must be available prior to the administration of Midazolam. Midazolam has more potential than the other benzodiazepines to cause respiratory depression and respiratory arrest. Side Effects: Laryngospasm, bronchospasm, dyspnea, respiratory depression and arrest, drowsiness, altered mental status, amnesia, bradycardia, tachycardia, premature ventricular contractions, and retching. Interactions: The effects of Midazolam can be accentuated by CNS depressants such as narcotics and alcohol. Dosage and administration Adults: For sedation – 2.0-2.5 mg slow IV over 2-3 minutes. May be repeated to max of 0.1mg/kg Peds: Not recommended
(Versed)
Sedative and Hypnotic
Midazolam is a benzodiazepine with strong hypnotic and amnestic properties.
Midazolam is a potent but short-acting benzodiazepine used as a sedative and hypnotic. It is three to four times more potent than Diazepam. Its onset of action is approximately 1.5 minutes when administered IV. Midazolam has impressive amnestic properties, and like other benzodiazepines, it has no effect on pain.
Midazolam is used as a premedication before cardioversion and other painful procedures.
Known hypersensitivity, narrow angle glaucoma, shock, depressed vital signs, and alcoholic coma.
Emergency resuscitative equipment must be available prior to the administration of Midazolam. Midazolam has more potential than the other benzodiazepines to cause respiratory depression and respiratory arrest.
Laryngospasm, bronchospasm, dyspnea, respiratory depression and arrest, drowsiness, altered mental status, amnesia, bradycardia, tachycardia, premature ventricular contractions, and retching.
The effects of Midazolam can be accentuated by CNS depressants such as narcotics and alcohol.
Dosage and administration
Random topics of interest, not in lectures yet 1/11/09 ACE inhibitor (ACEI) blocks conversion of angiotensin I to angiotensin 2 – results in lowering of BP, used to treat HTN & CHF.(Mechanism of Action: inhibits angiotensin converting enzyme, interfering w/ conversion of angiotensin I to angiotensin II) RAAS Vasopressin Calcium Channel Blocker (CCB) Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. Pituitary Krebs cycle Diuretic Fremitus Uremiais a term used to loosely describe the illness accompanying kidney failure (also called renal failure), in particular the nitrogenous waste products associated with the failure of this organ. In kidney failure, urea and other waste products, which are normally excreted into the urine, are retained in the blood. Early symptoms include anorexia and lethargy, and late symptoms can include decreased mental acuity and coma. It is usually diagnosed in kidney dialysis patients when the glomerular filtration rate, a measure of kidney function, is below 50% of normal.[2] Tetany – is a medical sign, the involuntary contraction of muscles, caused by diseases and other conditions that increase the action potential frequency. The muscle cramps caused by the disease tetanus are not classified as tetany; rather, they are due to a blocking of the inhibition to the neurons that supply muscles. Motor_end_plate Cushing’s Triad Pnuemonia Pulmonary embolism (PE)
Random topics of interest, not in lectures yet
1/11/09
In kidney failure, urea and other waste products, which are normally excreted into the urine, are retained in the blood. Early symptoms include anorexia and lethargy, and late symptoms can include decreased mental acuity and coma. It is usually diagnosed in kidney dialysis patients when the glomerular filtration rate, a measure of kidney function, is below 50% of normal.[2]
1/7/09 (UPDATED 1/11/08 RSI (Rapid sequence intubation) Indications: Trauma with GCS of <9, with gag reflex or significant facial trauma Closed head injury – major stroke Burn patients Any patient who can’t maintain an airway, still has gag reflex,- with possibility of successful intubation 6 ps Prep Preoxygenate, sat at 100% (do not bag while patient is under, all sphincters are relaxed) Pretreat (medicating) LOAD Lidocaine – 1-1.5 mg/kg (suppress gag reflex – gag can increase ICP) (Opiods – Fentanyl 3mcg/kg IV – decrease sympathetic response – also for AA or ICP) Atropine –0.02 mg/kg – decreases parasympathetic response (also decreases brady affect of Succinylcholine- especially peds) (Defasiculating dose – 10% of normal dose (non-depolarizing) – 2-5 minutes before Succinylcholine)( Vecuronium 0.1mg/kg) - Induction (sedation) Etomidate – 0.3 mg/kg Rapid onset – 15-45 sec Short duration – 3-12 min Midazolam (Versed) – 0.1-0.3 mg/kg – usual dose is 2 mg because causes hypotension 30-60 sec onset 15-30 minute duration Amnesic effects Paralysis (not performed in NYS by paramedics) Bind to ACH nicotinic receptors Depolarizing Succinylcholine (sux) – binds to Ach receptors blocking contraction of muscle 1-2mg/kg – max 150mg Peds 1-1.5mg/kg Hyperkalemia (renal problems, significant muscle damage, burn patients, ) Bradycardia Dysrythmias hypertension Non-depolarizing Do not cause fasciculations Longer onset Longer action Paralyzed patient has no definitive airway Must be ventilated manually throughout duration of paralysis No affect on mental status – MUST sedate Placement of tube Post intubation management
1/7/09 (UPDATED 1/11/08
RSI (Rapid sequence intubation)
6 ps
1/5/09 – NEEDS WORK! Plasma –% of blood Formed elements ` Albumins? RBC carry o2 via their hemoglobin 1 cubit mm contain 3 million RBC Thrombocytes – platelets – WBC- Neutrophils – active phagocytes , first to arrive at scene of injury (50-70% of wbc) Lymphoctes – (20-30% of wbc) Monocytes Plasma -92% water, plasma proteins are biggest contribs to osmosis Lymph = interstitial fluid To be continued…
1/5/09 – NEEDS WORK!
Plasma –% of blood
Plasma -92% water, plasma proteins are biggest contribs to osmosis
Lymph = interstitial fluid
To be continued…
1/5/2009 Cell membranes and other goodies Phospholipid bilayer Hydrophilic – inside Hydrophobic – towards outside Solubility – Lipid soluble will pass through easily Size of the particle Proteins or glucose – larger Ions and electrolytes- smaller (Insulin permits glucose to cross the membrane) Passive transport Aqueous environment Solution – liquid + electrolytes or ions (solvent + solute) Suspension – liquid + non electrical (proteins) Diffusion Simple diffusion will allow solutes to cross membrane if conditions are met Sodium & potassium ‘leak’ through (sodium potassium exchange pump recaptures the ‘escaped’ ions) (60-100 times per min) PVC – sodium leaking Filtration – substances moving across semi permeable membrane under influences of hydrostatic pressure Osmosis
1/5/2009
Cell membranes and other goodies
Phospholipid bilayer
(Insulin permits glucose to cross the membrane)
Passive transport
Diffusion
