Drugs affecting the CNS:
Benzodiazepines: Benzodiazepines (-pam/-lam) are a class of drugs that work by targeting GABA receptors in the CNS. GABA is the main inhibitory neurotransmitter in the CNS. When benzodiazepines bind to GABA receptors, Chloride is forced through the cell. This influx of Chloride causes hyperpolarizaion of the cell, and inhibits action potential, thus slowing neurotransmission. These drugs are used for management of anxiety, and as a treatment for stopping active seizures.
Actions:
Anti-anxiety
Sedative/hypnotic
Anterograde amnesia
Muscle relaxant
anticonvulsant
Side effects:
Drowsiness
Confusion
Respiratory depression
The antidote for reversal of overdose is Flumazenil
Barbiturates: These also target GABA receptors and work essentially the same as benzodiazepines do to slow neurotransmission.
Drug example: Phenytoin.
Actions:
Anti-anxiety
Sedative/hypnotic
Anterograde amnesia
Muscle relaxant
anticonvulsant
Side effects:
Drowsiness
Confusion
Respiratory depression
***Severe withdrawal from long term use***
Can have lethal interaction if taken with ETOH.
SSRIs: Selective Serotonin reuptake inhibitors. These drugs block reuptake of serotonin at the synapse, allowing for more free levels of serotonin and a prolonged action from this neurotransmitter. These drugs are used almost exclusively in treating depression and typically must be taken for 2-6weeks to reach therapeutic range. There is usually no significant withdrawal or major side effects with these drugs.
TCAs: Tricyclic antidepressants. These are an older class of drugs, but they are still utilized in treating refractory major depression and some psychoses. They work by blocking the reuptake of serotonin and norepinephrine at the synapse. They also block histamine receptors, muscarininc receptors, and adrenergic receptors, which can produce severe side effects in overdoses.
Side effects:
Tachycardia (in overdose can cause V-Tach and refractory V-fib)
Blurred vision
Urinary retention
Constipation
Monamine Oxidase Inhibitors: Monoamine oxidase is an enzyme found in the liver and the stomach. The body uses it to deactivate excess neurotransmitters. These can have lethal interactions with food containing tyrosine.
Antipsychotics: These are first line drugs for schizophrenia. They work by blocking D2 receptors in the brain and peripheral nerves (Dopamine). Studies have also demonstrated inhibitory effects against serotonin.
Uses:
Schizophrenia
Drug induced N/V
Opioids: These drugs mimic the action of opium, by attaching to Mu receptors in the CNS blocking transmission of pain signals in the spinal cord, in order to reduce pain signals from peripheral nerves.
Actions:
Analgesic
Antitussive (cough suppressant)
Respiratory depression
Antidote is Naloxome.
NSAIDS: Block COX-2 enzymes, inhibiting prostaglandin synthesis. Targets and reduces inflammatory response at the site of an injury.
Drugs affecting the cardiovascular system:
Beta-blockers and calcium channel blockers: Beta blockers work by targeting and inhibiting action at beta-2 adrenergic receptor sites. The result is a decrease in HR, and decrease in conduction speed of electrical impulses through the heart. These drugs are primarily used to treat hypertension, and tachydysrhythmias such as A-fib. Calcium channel blockers work by prolonging the plateau phase of the cardiac conduction cycle.They reduce the contractility of cardiac myocytes, and reduce the contractility of vascular smooth muscle. These are used in situations where we want to address contractility and thus reduce hypertension or dysrhythmia. Calcium channel blockers, particularly diltiazem, also reduce the rate of conduction through the AV node, making them a good choice for dealing with SVT or A-Fib.
Beta blocker suffix: -Lol
CCB suffix: -Dipine
ACE inhibitors: These work by preventing angiotensin converting enzyme from converting angiotensin 1 into angiotensin 2 in the lungs. This prevents systemic vasoconstriction, and inhibits the release of aldosterone from the adrenal cortex; thus preventing sodium reptake in the nephron. The result is reduction in systemic blood pressure. These are obviously used to treat hypertension.
ACE inhibitor suffix: -Pril
Angiotensin Receptor Blockers: Work by blocking angiotensin receptors, reducing angiotensin 1 to angiotensin 2 conversion. This reduces vasoconstriction and reduces sodium reuptake in the nephron, thus reducing BP.
Anti-arrhythmics:
These drugs deal with the movement of ions during the cardiac conduction cycle. In Phase 0, K+ transiently leaks out of the cell. Electrical stimulation from an incoming impulse triggers the opening of fast Na+ channels, leading to depolarization (the QRS complex). This peaks at phase 1. Next comes phase 2. Here there is still an efflux of K+ and voltage gated Ca+ channels open allowing an influx of Ca+. This is represented by the plateau phase. In phase 3 we have rapid repolarization as Ca+ channels close and K+ slow channels open. At phase 4 we return to resting potential.
Adenosine: Adenosine is indicated for treatment of SVT. It works by slowing conduction through the AV node and interrupts re-entry pathways, restoring normal sinus rhythm. It accomplishes this by blocking K+ in the cardiac conduction system.
Amiodarone: Used in the treatment of stable ventricular tachycardia. It works by blocking K+ channels, prolonging action potential, and prolonging the refractory period. This drug must be avoided in the case of severe CHF or cardiogenic shock.
Vasopressors: Vasopressors are a class of drug used to maintain perfusion of the tissues during times of hypotension. The goal is to maintain a MAP of 65mmHg. These drugs work by utilizing an adrenergic response (sympathomimetics) to cause increase in BP and CO, in order to raise MAP.
Dopamine: Dopamine works by stimulating alpha and beta receptors to cause increase HR, SV, and vasoconstriction. This raises systemic BP and MAP in patients who are severely hypotensive, usually secondary to bradycardia.
Other vasopressors used by some services include: -Levophed -Dobutamine -Epinephrine
Immunosuppressants: These drugs are used with patients who have autoimmune conditions or certain cancers. They work to suppress immune response.
Dexamethasone: This is a steroid drug that works to inhibit leukocyte infiltration and limit immune response. This is also used in cases of severe asthma.
Diuretics: A number of these medications exist, but the most common one is usually lasix. They work by blocking reabsorption of Na+ in the nephron, thus excreting more fluid in the form of urine. Some varieties are: Loop diuretics, and Potassium sparing diuretics. They are used to treat HTN, and CHF.
Overdoses and Toxidromes:
Opioids: Probably the most commonly encountered Tox drugs we run into in the prehospital field. Opioids stimulate the Mu receptors in the brain and are GABA agonists. They produce a state of euphoria, and are used clinically to block pain impulses at the spinal cord. When abused, overdose is common and presents with a very specific symptom set:
Altered LOA/LOC
Respiratory depression (usually <6/min)
Pupillary constriction
Treatment: Provide PPV if patient is apneic, and administer naloxone.
Stimulants: Cocaine, amphetamines, and many designer drugs fall into this category. They work by binding to adrenergic receptors for dopamine, serotonin, epi, and norepinephrine, to produce an adrenergic response. A major threat is that these drugs also block sodium channels in the cardiac system, which can lead to widening of the QRS, and the potential for ventricular tachycardia. Cardiac arrest is a very real possibility with these drugs. Overdose can also deplete the body's glycogen stores leading to rhabdomyolysis, MSOD, STEMI, etc. Symptoms include:
Agitation/delirium
Tachycardia (wide complex possible)
Dilated pupils
Hot dry skin
Possible chest pain
Possible dyspnea
Treatment is in the form of benzodiazepine administration, managing ABCs, and addressing hyperthermia. 12 Lead ECG should be performed to assess for ischemia.
Carbon monoxide poisoning: CO is an odourless and tasteless gas that is a byproduct of burning hydrocarbons. It has a 200x greater affinity for hemoglobin than does Oxygen, which means it can bind to RBCs and displace O2 from the circulating blood volume. This obviously leads to hypoxemia, and potentially can be fatal at high enough levels. This gas is often used in suicide attempts, by running a vehicle in an enclosed space, but it is also accidentally inhaled in residential settings and house fires. A good indication that CO may be the cause of your patient's symptoms, would be to look for a source. Most services carry CO detectors, so it should become evident quickly if there is a CO leak.
Symptoms include:
General flu-like unwellness
Nausea
altered LOA/LOC
Headache
Tachypnea
Treatment is 100% O2 and transport to the ED.
ASA overdose: ASA is a component of a number of OTC medications and can be easily overdosed on if several are taken together accidentally. Additionally, there exists a product called Oil of Wintergreen, which contains an extremely high level of ASA. This is a drug with a high potential for accidental overdose. ASA overdose causes a state of metabolic acidosis, and stimulates an increased respiratory drive. The increase in respirations ultimately leads to respiratory alkylosis The kidneys respond to acidosis by dumping H+ in the urine, leading to significant fluid loss, and loss of electrolytes. Unfortunately acidosis also impairs glucose conversion, which leads the cells of the body to switch to anaerobic metabolism, thus creating further acidosis. A third problem, for which the mechanism is not totally clear, is the onset of cerebral edema.
Treatment is a bit above the PCP pay grade:
Maintain MAP of 65 CAUTIOUSLY. These patients have cerebral edema, and we dont want to exacerbate that with excess fluid. I would say patch the BHP.
Dextrose to address hypoglycemia
PPV to attempt to improve ventilation.
Be prepared for seizure
Acetaminophen overdose: Acetaminophen is toxic to the liver in doses >4000mg/24hrs (adult). Presentation will vary depending on the timeline since ingestion.
Mild injury: 30min – 24 hrs: N/V, Pallor, Fatigue.
Moderate injury: RUQ pain.
Severe injury: RUQ pain, Jaundice, confusion, hypoglycemia, death.
Treatment: MUST BE CAUGHT EARLY. N-Acetylcystine.
Beta-Blocker Overdose: Beta-blockers work by inhibiting beta 1 adrenergic receptors. This means a decrease in cardiac contractility and heart rate. This is desirable in treating HTN and tachydysrhythmias. However, in cases of overdose, we see a blockade of beta 2 receptors as well, which ultimately leads to brochoconstriction; which could be deadly in COPD/Asthma patients, or those with multiple comorbidities. Additionally, beta-blocker overdose impairs glycolysis, which means the body cannot access its glycogen stores for energy. This can lead to hypoglycemia. Overdose may produce:
Bradycardia
Hypotension
Heart blocks
Bronchoconstriction
Hypoglycemia
Treatment:
Fluids to maintain MAP of 65
Glucagon may be patched for as it bypasses the adrenergic receptors and stimulates the myocytes to increase cardiac output.
Dextrose to correct hypoglycemia. We do have to be careful here because dextrose, and the insulin response, can shift K+ out of cells and into the extracellular environment. This leads to potential for hypokalemia. A patch to the BHP may be warranted to consult on these patients.
CCB Overdose: CCBs work by blocking calcium channels, to decrease contractility and dromotropy in cardiac myocytes. In the case of overdose we have a very exaggerated version of this mechanism, leading to severe decreases in contractility and conduction. This will lead to hypotension, QRS widening due to conduction delays, and an overall drop in MAP.
Treatment:
Fluids
Calcium if you carry it
Glucagon
Organophosphates:
These overdoses are pretty rare, but they may occur in rural settings where organophosphates are still used as pesticides. These drugs cause a massive cholinergic response in the body. Symptoms include SLUDGE and the Killer Bs.
S- Salivation
L-Lacrimation
U-Urination
D-Defecation
G-GI upset
E-Emesis
B-Bradycardia
B-Brochorrhea
B-Bronchoconstriction
Treatment is Atropine.
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