question: What in particular does Atropine do to the body when being used for treating bradycardia ?
comment: Bradycardia is in part mediated by the parasympathetic response of the vagus nerve. This releases acetylcholine onto muscarinic acetylcholine receptors in the heart, which slows it down. Atropine can treat bradycardia by acting as a competitive antagonist of the receptors, blocking the chemical from keeping the heart rate low. Fun fact: the existence of neurotransmitters were proven with an experiment with two frog hearts and acetylcholine (then termed "VAGUSSTOFF" by the German scientist, literally "vagus stuff"). The exact workings are complex, but Otto Loewi reportedly came up with the experiment after dreaming about it, and got out of bed in the middle of the night because it is thought he had once theorized the trial but then forgot it. The experiment involved stimulating the vagus nerve of a heart in one chamber and observing it slowed when electrically stimulated. There was a second heart in a second chamber. Both chambers were connected and saline was present as a fluid in both. When the first heart slowed, the second heart also slowed, indicating the presence of some medium that could affect the second heart through the saline. This chemical was identified as acetylcholine.
passages: In overdoses, atropine is poisonous. Atropine is sometimes added to potentially addictive drugs, particularly antidiarrhea opioid drugs such as diphenoxylate or difenoxin, wherein the secretion-reducing effects of the atropine can also aid the antidiarrhea effects.
  
  Although atropine treats bradycardia (slow heart rate) in emergency settings, it can cause paradoxical heart rate slowing when given at very low doses (i.e. <0.5 mg), presumably as a result of central action in the CNS. One proposed mechanism for atropine's paradoxical bradycardia effect at low doses involves blockade of inhibitory presynaptic muscarinic autoreceptors, thereby blocking a system that inhibits the parasympathetic response.
   There is also some vagal innervation of the atrial muscle, and to a much lesser extent, the ventricular muscle. Vagus activation, therefore, results in modest reductions in atrial contractility (inotropy) and even smaller decreases in ventricular contractility.
  
  Muscarinic receptor antagonists bind to muscarinic receptors thereby preventing ACh from binding to and activating the receptor. By blocking the actions of ACh, muscarinic receptor antagonists very effectively block the effects of vagal nerve activity on the heart. By doing so, they increase heart rate and conduction velocity.
  
  Section::::History.
   Atropine was previously included in international resuscitation guidelines for use in cardiac arrest associated with asystole and PEA, but was removed from these guidelines in 2010 due to a lack of evidence for its effectiveness. For symptomatic bradycardia, the usual dosage is 0.5 to 1 mg IV push, may repeat every 3 to 5 minutes up to a total dose of 3 mg (maximum 0.04 mg/kg).
   In cardiac uses, it works as a nonselective muscarinic acetylcholinergic antagonist, increasing firing of the sinoatrial node (SA) and conduction through the atrioventricular node (AV) of the heart, opposes the actions of the vagus nerve, blocks acetylcholine receptor sites, and decreases bronchial secretions.
   Atropine is also useful in treating second-degree heart block Mobitz type 1 (Wenckebach block), and also third-degree heart block with a high purkinje or AV-nodal escape rhythm. It is usually not effective in second-degree heart block Mobitz type 2, and in third-degree heart block with a low Purkinje or ventricular escape rhythm.
  
  Atropine has also been used in an effort to prevent a low heart rate during intubation of children; however, evidence does not support this use.
  
  Section::::Medical uses.:Secretions.
   Atropine's actions on the parasympathetic nervous system inhibit salivary and mucus glands. The drug may also inhibit sweating via the sympathetic nervous system. This can be useful in treating hyperhidrosis, and can prevent the death rattle of dying patients. Even though atropine has not been officially indicated for either of these purposes by the FDA, it has been used by physicians for these purposes.
  
  Section::::Medical uses.:Poisonings.
   BULLET::::- Atropine — The process of intubation can cause massive stimulation to vagus nerve, causing bradycardia (low heart rate). The people who are at increased risk of bradycardia are neonates and children. This does not happen in adults because sympathetic stimulation overpowers the vagal response. However, for those adults who have received drugs such as beta blocker, calcium channel blocker, and digoxin has an increased risk of developing bradycardia. Atropine is a muscarinic receptor antagonist, thus blocking the vagal response. The dose is 0.01 mg/kg. It has quick onset of action, and common side effects are: increased heart rate, dry mouth, flushing, and urinary retention.
   ANP binds to a specific set of receptors – ANP receptors. Receptor-agonist binding causes the increase in renal sodium excretion, which results in a decreased ECF and blood volume. Secondary effects may be an improvement in cardiac ejection fraction and reduction of systemic blood pressure.
  
  Section::::Physiological effects.:Renal.
  
  ANP acts on the kidney to increase sodium and water excretion (natriuresis) in the following ways:
   General systemic adverse effects are due to the pharmacological effects of the anesthetic agents used. The conduction of electric impulses follows a similar mechanism in peripheral nerves, the central nervous system, and the heart. The effects of local anesthetics are, therefore, not specific for the signal conduction in peripheral nerves. Side effects on the central nervous system and the heart may be severe and potentially fatal. However, toxicity usually occurs only at plasma levels which are rarely reached if proper anesthetic techniques are adhered to. High plasma levels might arise, for example, when doses intended for epidural or intrasupport tissue administration are accidentally delivered as intravascular injection.
   Theophylline was originally used as a bronchodilator, although its usage has declined due to several side effects such as seizures and cardiac arrhythmias caused by adenosine A1 receptor antagonism.
  
  BULLET::::- Herbal medicine
  
  Several herbs used in Traditional Chinese medicine contain drug compounds that are antagonists of P2X purinoreceptors. The following table provides an overview of these drug compounds and their interaction with purinergic receptors.
  
  BULLET::::- Vasodilators
   Since the actions of BNP are mediated via the ANP receptors, the physiologic effects of BNP are identical to those of ANP. Those will be reviewed here.
  
  Receptor-agonist binding causes a reduction in renal sodium reabsorption, which results in a decreased blood volume. Secondary effects may be an improvement in cardiac ejection fraction and reduction of systemic blood pressure. Lipolysis is also increased.
  
  Section::::Physiologic effects.:Renal.
   Section::::Side effects.:Bronchospasm.
  
  Bronchospasm has been reported on occasion with the use of atracurium. However, this particular undesirable effect does not appear to be observed nearly as often as that seen with rapacuronium, which led to the latter's withdrawal of approval for clinical use worldwide.
   Section::::Muscle relaxants.:Adverse effects.
  
  BULLET::::- Depolarizing Muscle Relaxants i.e. Suxamethonium
  
  BULLET::::- Hyperkalemia – A small rise of 0.5 mmol/l occurs normally, this is of little consequence unless potassium is already raised such as in renal failure
  
  BULLET::::- Hyperkalemia – Exaggerated potassium release in burn patients (occurs from 24 hours after injury, lasting for up to 2 years), neuromuscular disease and paralyzed (quadraplegic, paraplegic) patients. The mechanism is reported to be through upregulation of acetylcholine receptors in those patient populations with increased efflux of potassium from inside muscle cells. May cause life-threatening arrhythmia
   Common side effects include muscle cramps, stuffy nose, cough, and high blood potassium. Severe side effects may include angioedema, low blood pressure, and kidney problems. Use during pregnancy may result in harm to the baby. Use is not recommended during breastfeeding. It is in the angiotensin receptor blocker family of medication. It works by blocking angiotensin II.
   Atropine eye drops have been shown to be effective in slowing the progression of myopia in children in several studies, but it is not available for this use, and side effects would limit its use.
  
  Section::::Medical uses.:Heart.
  
  Injections of atropine are used in the treatment of bradycardia (a heart rate  60 beats per minute).
   Atropine is contraindicated in patients pre-disposed to narrow angle glaucoma.
  
  Section::::Chemistry.
   A profound depression of brain functions may occur at even higher concentrations which may lead to coma, respiratory arrest, and death. Such tissue concentrations may be due to very high plasma levels after intravenous injection of a large dose.
  
  Another possibility is direct exposure of the central nervous system through the cerebrospinal fluid, i.e., overdose in spinal anesthesia or accidental injection into the subarachnoid space in epidural anesthesia.
  
  Section::::Side effects.:Potential side effects.:Cardiovascular system.
   Systemic exposure to excessive quantities of ropivacaine mainly result in central nervous system (CNS) and cardiovascular effects – CNS effects usually occur at lower blood plasma concentrations and additional cardiovascular effects present at higher concentrations, though cardiovascular collapse may also occur with low concentrations. CNS effects may include CNS excitation (nervousness, tingling around the mouth, tinnitus, tremor, dizziness, blurred vision, seizures followed by depression (drowsiness, loss of consciousness), respiratory depression and apnea). Cardiovascular effects include hypotension, bradycardia, arrhythmias, and/or cardiac arrest – some of which may be due to hypoxemia secondary to respiratory depression.
  
  Section::::Clinical use.:Postarthroscopic glenohumeral chondrolysis.
   There is also a soluble guanylyl cyclase that cannot be stimulated by ANP. Instead, vascular endothelial cells will use L-arginine to make nitric oxide via nitric oxide synthase. The nitric oxide will then diffuse into the vascular smooth muscle and will activate the soluble guanylyl cyclase. The subsequent increase in cGMP will cause vasodilation with the same effects as described above. This is why nitroglycerine is given to a person having a heart attack. The nitroglycerine will be metabolized to nitric oxide, which will stimulate soluble guanylyl cyclase. This will result in a decrease in total peripheral resistance and a decrease in preload on the heart. As a result, work done by the heart will decrease and will allow the heart to contract less strongly. Weaker contractions will lead to more blood flow in the coronary arteries, which will help the ischemic cardiac myocytes.
   Clinically significant adverse events result from systemic absorption of bupivacaine and primarily involve the central nervous system (CNS) and cardiovascular system. CNS effects typically occur at lower blood plasma concentrations. Initially, cortical inhibitory pathways are selectively inhibited, causing symptoms of neuronal excitation. At higher plasma concentrations, both inhibitory and excitatory pathways are inhibited, causing CNS depression and potentially coma. Higher plasma concentrations also lead to cardiovascular effects, though cardiovascular collapse may also occur with low concentrations. Adverse CNS effects may indicate impending cardiotoxicity and should be carefully monitored.
   Common side effects include headache, slow heart rate, and anxiety. Other side effects include an irregular heartbeat. If it leaks out of the vein at the site it is being given, norepinephrine can result in limb ischemia. If leakage occurs the use of phentolamine in the area affected may improve outcomes. Norepinephrine works by binding and activating alpha adrenergic receptors.
   These drugs work by increasing nitric oxide levels in the blood and inducing coronary vasodilation which will allow for more coronary blood flow due to a decreased coronary resistance, allowing for increased oxygen supply to the vital organs (myocardium). The nitric oxide increase in the blood resulting from these drugs also causes dilation of systemic veins which in turn causes a reduction in venous return, ventricular work load and ventricular radius. All of these reductions contribute to the decrease in ventricular wall stress which is significant because this causes the demand of oxygen to decrease. In general organic nitrates decrease oxygen demand and increase oxygen supply. It is this favourable change to the body that can decrease the severity of ischemic symptoms, particularly angina.
   Sodium nitroprusside
  
  Sodium nitroprusside (SNP), sold under the brand name Nitropress among others, is a medication used to lower blood pressure. This may be done if the blood pressure is very high and resulting in symptoms, in certain types of heart failure, and during surgery to decrease bleeding. It is used by continuous injection into a vein. Onset is typically immediate and effects last for up to ten minutes.
   Naproxcinoid is metabolized to naproxen and a nitric oxide donating moiety. NO has various cardiovascular effects, including vasodilatory and platelet-inhibitory actions as well as the inhibition of vascular smooth muscle proliferation that serves to maintain normal vascular tone.
  
  Section::::Safety profile.
  
  Section::::Safety profile.:Blood pressure profile.
   Atropine acts on the M2 receptors of the heart and antagonizes the activity of acetylcholine. It causes tachycardia by blocking vagal effects on the sinoatrial node. Acetylcholine hyperpolarizes the sinoatrial node, which is overcome by MRA and thus increases the heart rate. If atropine is given by intramuscular or subcutaneous injection, it causes initial bradycardia. This is because by i.m/s.c it acts on presynaptic M1 receptors (autoreceptors). Intake of acetylcholine in axoplasm is prevented and the presynaptic nerve releases more acetylcholine into the synapse that initially causes bradycardia.
  