Coffee and Arrhythmias
For all you coffee drinkers out there that are concerned it is costing your heart some trouble...have no fear for a new large survey is here.
Brought on by the common concern that caffeine can make one's "heart flutter" researchers at Kaiser Permanente in Oakland, California decided to look into the amount of hospitalizations that java drinkers have versus those that avoid it altogether. They have found that coffee is not a determining factor for heart hospitalizations....so keep chugging away.
Not only does coffee not send you to the hospital clutching your chest but evidence from this research show that it may keep you from making that trip! The study began in the 1970s and 1980s with 130,000 men and women ranging in age from 18 to 90 years old. Compared with those that avoid coffee altogether, of those drinking 4+ cups per day were 18% less likely to be hospitalized for heart arrhythmia. Those drinking 1-3 cups were only 7% less likely to be hospitalized.
You may be wondering about the other lifestyle choices these 130,000 people made such as smoking. The researchers found that even when smoking status, gender, weight, cardiac history and education differences were all taken into account, the 4+ cups of coffee a day still kept them from a trip to the hospital for their heart. One blogger disagrees with the results: "I do not blame coffee intake FOR the arrhythmia but I do blame it for drastically making it worse. Last year, I gave up coffee for Lent. After three weeks, the arrhythmia was almost gone." So is this one person that blogged about this the exception or are there others like him?
Coffee and Strokes
Not long after the discovery was released about coffee not linked to arrhythmias it was determined that coffee was also associated with lower stroke risk! The study began in the mid 1990s with health records of more than 20,000 European men and women between 39 and 79 years old. The research was done at the University of Cambridge in England with people that were free of stroke history, heart disease and cancer in the mid 1990s. There were 855 strokes in these 120,000 people over the next 12 years. As it turns out though, coffee drinkers (drip grind, decaffeinated or even lowly instant) were only 71 percent as likely to have had a stroke as those that avoided the java. Smoking, physical activity, weight, tea drinking, blood pressure and cholesterol were all taken into account in this research.
This research did not seem to be dose-dependent: those that drank one cup of coffee a day or four had the same percentage of fewer strokes. Even with these results, the mechanism of action is unknown. There have even been some studies showing that because of the high antioxidant amounts in coffee, it improves insulin sensitivity and glucose metabolism. Thus, it is beneficial for those with diabetes by improving the body's response to insulin! Why is drinking coffee associated with lower stroke risk, less hospitalizations due to arrhythmias and better insulin sensitivity? Is it truly a miracle drug after all?
The coffee and arrhythmia link: http://www.sciencenews.org/view/generic/id/56862/title/Coffee_not_linked_to_heart_arrhythmia
The coffee and stroke link: http://www.sciencenews.org/view/generic/id/56701/title/Coffee_associated_with_lower_stroke_risk
Wednesday, June 23, 2010
Friday, June 18, 2010
How and what do Potassium and Calcium Channel Blockers block?
Many patients may hear that the medication that their doctor is prescribing them is a sodium channel blocker, Beta-blocker, potassium channel blocker, or a calcium channel blocker without being told what the difference is or why or how they work so well. Patients may be wondering...is Beta the letter of my fraternity that has come back to haunt me after all these years? As shown in the previous blog and will be further represented in this blog, sodium, "Beta", potassium and calcium are not some evil little molecules out to get your heart. They are very vital aspects of your bodily functions but can sometimes become overstimulated, cause arrhythmias and those funky channel blockers become just what the doctor orders. In the previous blog, I reviewed Sodium and Beta channel blockers. Here I will discuss Potassium and Calcium Channel blockers.
Class III: Potassium Channel Blockers
Action Potentials and the Role Potassium Plays in Action Potentials
Remember the action potentials discussed with the sodium channels? The beginning of the action potential starts with the depolarization of the cell membrane when sodium rushes in. The cell begins to repolarize when potassium leaves the cell, although not as quickly as the sodium rushes in. This repolarization brings the cell membrane back down to a more negative resting potential.
What a Potassium Channel Blocker Blocks and What They are Used for Treating
Potassium Channel Blockers bind to and block the potassium channels that are responsible for the cell membrane repolarization. Blocking these channels slows (delays) repolarization, which leads to an increase in action potential duration and an increase in the effective refractory period. An increase in the refractory period means the period of time that the cell is unexcitable and therefore cannot receive another action potential is prolonged. On an electrocardiogram, this delay of the depolarization increases the QT interval.
By making the cell less excitable, Potassium Channel Blockers are very effective in treating tachycardias. They are also known to treat supraventricular and ventricular arrythmias, atrial fibrillation, and atrial flutter.
Examples of Potassium Channel Blockers and Their Side Effects
Amiodarone, Dronedarone, Bretylium, Ibutilide, Dofetilide
The side effects of Potassium Channel Blockers are to produce a type of ventricular tachycardia, bradycardia and atrioventricular block or SA node dysfunction. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Class IV: Calcium Channel Blockers
What are Calcium Channels and Where are They Found
Calcium channels are cells known as "excitable cells" that are sensitive to electrical impulses. Like the sodium and potassium channels, when the proteins receive the correct signal, the channel opens, allowing calcium to flow across the channel. The small charge that the calcium ion carries can stimulate muscle contractions, hormone release or firing of a neurotransmitter. Therefore, calcium channels are found in muscles, glial cells and neurons.
What a Calcium Channel Blocker Blocks and What They are Used for Treating
Calcium Channel Blockers dilate the arteries in the heart, reducing blood pressure in the arteries which leads to the heart being able to pump blood more easily. Essentially the heart's need for oxygen to pump the heart is lowered because it does not need to pump as often.
Calcium channel blockers are often used for high blood pressure, chest pain (due to lack of oxygen in the heart), and arrhythmias such as atrial fibrillation, and supraventricular tachycardia. They can be used after a heart attack for a patient that is not a good candidate for beta-blockers. Unfortunately, calcium channel blockers have not been shown to prevent future heart attacks.
Examples of Calcium Channel Blockers and Their Side Effects
Amlodipine, Diltiazem (Brand=Cardizem), Felodipine, Nifedipine, Nicardipine, Nimodipine, Nisoldipine, Verapamil
The most common side effects of Calcium Channel Blockers are constipation, nausea, headache, rash, swelling, low blood pressure, drowsiness and dizziness. In addition, liver dysfunction, sexual dysfunction and overgrowth of gums may occur. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Class III: Potassium Channel Blockers
Action Potentials and the Role Potassium Plays in Action Potentials
Remember the action potentials discussed with the sodium channels? The beginning of the action potential starts with the depolarization of the cell membrane when sodium rushes in. The cell begins to repolarize when potassium leaves the cell, although not as quickly as the sodium rushes in. This repolarization brings the cell membrane back down to a more negative resting potential.
What a Potassium Channel Blocker Blocks and What They are Used for Treating
Potassium Channel Blockers bind to and block the potassium channels that are responsible for the cell membrane repolarization. Blocking these channels slows (delays) repolarization, which leads to an increase in action potential duration and an increase in the effective refractory period. An increase in the refractory period means the period of time that the cell is unexcitable and therefore cannot receive another action potential is prolonged. On an electrocardiogram, this delay of the depolarization increases the QT interval.
By making the cell less excitable, Potassium Channel Blockers are very effective in treating tachycardias. They are also known to treat supraventricular and ventricular arrythmias, atrial fibrillation, and atrial flutter.
Examples of Potassium Channel Blockers and Their Side Effects
Amiodarone, Dronedarone, Bretylium, Ibutilide, Dofetilide
The side effects of Potassium Channel Blockers are to produce a type of ventricular tachycardia, bradycardia and atrioventricular block or SA node dysfunction. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Class IV: Calcium Channel Blockers
What are Calcium Channels and Where are They Found
Calcium channels are cells known as "excitable cells" that are sensitive to electrical impulses. Like the sodium and potassium channels, when the proteins receive the correct signal, the channel opens, allowing calcium to flow across the channel. The small charge that the calcium ion carries can stimulate muscle contractions, hormone release or firing of a neurotransmitter. Therefore, calcium channels are found in muscles, glial cells and neurons.
What a Calcium Channel Blocker Blocks and What They are Used for Treating
Calcium Channel Blockers dilate the arteries in the heart, reducing blood pressure in the arteries which leads to the heart being able to pump blood more easily. Essentially the heart's need for oxygen to pump the heart is lowered because it does not need to pump as often.
Calcium channel blockers are often used for high blood pressure, chest pain (due to lack of oxygen in the heart), and arrhythmias such as atrial fibrillation, and supraventricular tachycardia. They can be used after a heart attack for a patient that is not a good candidate for beta-blockers. Unfortunately, calcium channel blockers have not been shown to prevent future heart attacks.
Examples of Calcium Channel Blockers and Their Side Effects
Amlodipine, Diltiazem (Brand=Cardizem), Felodipine, Nifedipine, Nicardipine, Nimodipine, Nisoldipine, Verapamil
The most common side effects of Calcium Channel Blockers are constipation, nausea, headache, rash, swelling, low blood pressure, drowsiness and dizziness. In addition, liver dysfunction, sexual dysfunction and overgrowth of gums may occur. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Tuesday, June 15, 2010
How and what do all of these medication Blockers block?
Many patients may hear that the medication that their doctor is prescribing them is a sodium channel blocker, Beta-blocker, potassium channel blocker, or a calcium channel blocker without being told what the difference is or why or how they work so well. Patients may be wondering...is Beta the letter of my fraternity that has come back to haunt me after all these years? As you will see, sodium, "Beta", potassium and calcium are not some evil little molecules out to get your heart. They are very vital aspects of your bodily functions but can sometimes become overstimulated, cause arrhythmias and those funky channel blockers become just what the doctor orders. For now, I will just review Sodium Channel Blockers and Beta Blockers. Please stay tuned for a future blog in which I will review Potassiam and Calcium Channel-Blockers.
Class I: Sodium Channel Blockers
Action Potentials & The Role Sodium Channels Play in Action Potentials
An action potential is a short-lasting event in which the electrical membrane potential of a cell rapidly rises and falls. These occur in excitatory cells, such as neurons. In muscle cells, an action potential is the first step in the chain of events leading to contraction. Action potentials are often referred to as "spikes" or a neuron "firing." They are generated by special types of voltage-gated ion channels spanning the cell membrane. When the cell is resting, the channels are closed and are inactive. But if the membrane potential increases to a defined threshold value, the channels quickly open and allow ion movement across the membrane. This opening of the ion channels allows sodium to move into the cell, which further increases the membrane potential. More sodium channels open as a result, producing a greater electrical current. When all of the sodium ion channels are open, the cell is now more positive on the inside than on the outside; therefore, positive charge will want to leave the cell to attempt to reach the original threshold value at the resting potential. Therefore potassium channels are opened and potassium is released from the cell and the cell returns to its resting potential.
What a Sodium Channel Blocker Blocks and What They are Used for Treating
Sodium channel blockers reduce the exitogenicity of the cell membranes. Usually the phase depolarization (the moment that sodium usually flows in quickly and causes the cell to become more positive) is depressed. This prolongs the action potential by slowing conduction and decreases conductivity.
Sodium channel blockers are used for treating atrial fibrillation(Class Ia), atrial flutter (Ia), supraventricular (Ia) and ventricular tachyarrhythmias (Class Ia & IIb & Ic).
Examples of Sodium Channel Blockers and Their Side Effects
Ia: Quinidine, Procainamide, Disopryamide
Ib: Lidocaine, Tocainide, Mexiletine, Phenytoin (Brand=Dilantin)
Ic: Flecainide, Propafenone, Moricizine
Side effects include: Tachycardia, dry mouth, urinary retention, blurred vision, constipation, diarrhea, nausea, headache, and dizziness. Of course, not all Sodium Channel blockers have all of these side effects. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Class II: Beta-Blockers
How Beta Receptors Normally Operate
Most people have experienced adrenaline rushes and know that it's a chemical that does some quite amazing things to our bodies. Adrenaline is also known as epinephrine and it acts by binding to receptors on the outside (membrane) of our cells. The receptors specialized for epinephrine are called Beta-adrenergic receptors and are made of 7 alpha helices spanning the cell membrane. Once epinephrine is bound to the receptor, the receptor is activated and a signal transduction cascade begins that ultimately stimulates the breakdown of glycogen for energy. First, the cytoplasmic loops (inside the cell) that connect the alpha helices together change their conformation. A β-adrenergic receptor mediates its effects via a class of peripheral membrane proteins known as the heterotrimeric G-proteins. It has 3 subunits, alpha (α), beta (β), and gamma (γ). In the inactive state, GDP is bound to the alpha subunit and when activated, this GDP molecule leaves and GTP takes its place. The beta-gamma dimer dissociates from the alpha subunit. This activation of the G protein activates adenylyl cyclase, which activates cyclic AMP (cAMP). cAMP bind to Protein Kinase A (PKA), activating PKA. PKA is a key regulator of the breakdown of glycogen and the body receives a sudden burst of energy!
What a Beta-Blocker Blocks and What They are Used for Treating
Beta-blockers are drugs that block norepinephrine and epinephrine (adrenaline) from binding to beta receptors on nerves. By blocking these neurotransmitters' effects, beta blockers reduce heart rate, reduce blood pressure by dilating blood vessels and may constrict air passages by stimulating the muscles that surround the air passages to contract. There are three types of beta receptor that control a variety of functions based on their location in the body. Beta-1 receptors are located in the heart, eye and kidneys; Beta-2 receptors are located in the lungs, GI tract, liver, uterus, blood vessels and skeletal muscle; Beta-3 receptors are located in fat cells. Beta blockers primarily block the Beta-1 and Beta-2 receptors.
Beta blockers are used for treating arrhythmia (irregular heart rhythms), high blood pressure, heart failure, chest pain (angina), tremors and sometimes prevention of migraines. They are also used after heart attacks to prevent further heart attacks.
Examples of Beta-blockers and Their Side Effects
As you will notice, the Beta-blockers listed below all end in "-lol."
Acebutolol
Atenolol
Bisoprolol
Carvedilol (Coreg)
Metoprolol (Toprol or Lopressor)
Nadolol
Pindolol
Propranolol
Sotalol
Timolol
The side effects of beta blockers may cause diarrhea, stomach cramps, nausea, vomiting, rash, blurred vision, muscle cramps, fatigue, headache, dizziness, confusion, depression, nightmares, hallucinations, shortness of breath in asthmatics and may cause low blood pressure. Of course, not all Beta-blockers have all of these side effects. Sudden withdrawal of Beta blockers may worsen chest pain and cause heart attacks. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Class I: Sodium Channel Blockers
Action Potentials & The Role Sodium Channels Play in Action Potentials
An action potential is a short-lasting event in which the electrical membrane potential of a cell rapidly rises and falls. These occur in excitatory cells, such as neurons. In muscle cells, an action potential is the first step in the chain of events leading to contraction. Action potentials are often referred to as "spikes" or a neuron "firing." They are generated by special types of voltage-gated ion channels spanning the cell membrane. When the cell is resting, the channels are closed and are inactive. But if the membrane potential increases to a defined threshold value, the channels quickly open and allow ion movement across the membrane. This opening of the ion channels allows sodium to move into the cell, which further increases the membrane potential. More sodium channels open as a result, producing a greater electrical current. When all of the sodium ion channels are open, the cell is now more positive on the inside than on the outside; therefore, positive charge will want to leave the cell to attempt to reach the original threshold value at the resting potential. Therefore potassium channels are opened and potassium is released from the cell and the cell returns to its resting potential.
What a Sodium Channel Blocker Blocks and What They are Used for Treating
Sodium channel blockers reduce the exitogenicity of the cell membranes. Usually the phase depolarization (the moment that sodium usually flows in quickly and causes the cell to become more positive) is depressed. This prolongs the action potential by slowing conduction and decreases conductivity.
Sodium channel blockers are used for treating atrial fibrillation(Class Ia), atrial flutter (Ia), supraventricular (Ia) and ventricular tachyarrhythmias (Class Ia & IIb & Ic).
Examples of Sodium Channel Blockers and Their Side Effects
Ia: Quinidine, Procainamide, Disopryamide
Ib: Lidocaine, Tocainide, Mexiletine, Phenytoin (Brand=Dilantin)
Ic: Flecainide, Propafenone, Moricizine
Side effects include: Tachycardia, dry mouth, urinary retention, blurred vision, constipation, diarrhea, nausea, headache, and dizziness. Of course, not all Sodium Channel blockers have all of these side effects. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Class II: Beta-Blockers
How Beta Receptors Normally Operate
Most people have experienced adrenaline rushes and know that it's a chemical that does some quite amazing things to our bodies. Adrenaline is also known as epinephrine and it acts by binding to receptors on the outside (membrane) of our cells. The receptors specialized for epinephrine are called Beta-adrenergic receptors and are made of 7 alpha helices spanning the cell membrane. Once epinephrine is bound to the receptor, the receptor is activated and a signal transduction cascade begins that ultimately stimulates the breakdown of glycogen for energy. First, the cytoplasmic loops (inside the cell) that connect the alpha helices together change their conformation. A β-adrenergic receptor mediates its effects via a class of peripheral membrane proteins known as the heterotrimeric G-proteins. It has 3 subunits, alpha (α), beta (β), and gamma (γ). In the inactive state, GDP is bound to the alpha subunit and when activated, this GDP molecule leaves and GTP takes its place. The beta-gamma dimer dissociates from the alpha subunit. This activation of the G protein activates adenylyl cyclase, which activates cyclic AMP (cAMP). cAMP bind to Protein Kinase A (PKA), activating PKA. PKA is a key regulator of the breakdown of glycogen and the body receives a sudden burst of energy!
What a Beta-Blocker Blocks and What They are Used for Treating
Beta-blockers are drugs that block norepinephrine and epinephrine (adrenaline) from binding to beta receptors on nerves. By blocking these neurotransmitters' effects, beta blockers reduce heart rate, reduce blood pressure by dilating blood vessels and may constrict air passages by stimulating the muscles that surround the air passages to contract. There are three types of beta receptor that control a variety of functions based on their location in the body. Beta-1 receptors are located in the heart, eye and kidneys; Beta-2 receptors are located in the lungs, GI tract, liver, uterus, blood vessels and skeletal muscle; Beta-3 receptors are located in fat cells. Beta blockers primarily block the Beta-1 and Beta-2 receptors.
Beta blockers are used for treating arrhythmia (irregular heart rhythms), high blood pressure, heart failure, chest pain (angina), tremors and sometimes prevention of migraines. They are also used after heart attacks to prevent further heart attacks.
Examples of Beta-blockers and Their Side Effects
As you will notice, the Beta-blockers listed below all end in "-lol."
Acebutolol
Atenolol
Bisoprolol
Carvedilol (Coreg)
Metoprolol (Toprol or Lopressor)
Nadolol
Pindolol
Propranolol
Sotalol
Timolol
The side effects of beta blockers may cause diarrhea, stomach cramps, nausea, vomiting, rash, blurred vision, muscle cramps, fatigue, headache, dizziness, confusion, depression, nightmares, hallucinations, shortness of breath in asthmatics and may cause low blood pressure. Of course, not all Beta-blockers have all of these side effects. Sudden withdrawal of Beta blockers may worsen chest pain and cause heart attacks. Talk with your doctor and your pharmacist to find out what the right drug is for you. And don't forget to rate the drug on www.RateaDrug.com to let others know what experiences you had with a specific medication!
Friday, June 11, 2010
Existing Pharmacological Treatments for Arrhythmia
Pharmacological treatment includes administering antiarrhythmic medications like the ones listed on this page in addition to hundreds of others. A complete list of antiarrhyhmic medications can be seen on http://rateadrug.com/Arrhythmia-Irregular-Heartbeat-symptoms-feedback.aspx . Normally because antiarrhythmic agents have a narrow toxic-therapeutic relationship, important compications of therapy can results from amounts of drug that only slightly exceed the amount necessary to produce beneficial effects. It is obvious that careful dosage is essential to maintain adequate but nontoxic amounts of drug in the body. There are many factors to consider when prescribing an antirarrhythmic medication: tissue type, the degree of acute or chronic damage, heart rate, membrane potential, heart rate, intrinsic tissue properties, orientation of myocardial fibers and other associated conditions. It therefore may take multiple attempts for a doctor to find the medication that is right for the patient. Tachycardias (beating too fast) and premature beats may be administered intravenously in an emergency situation or orally for long term treatment. Antiarrhythmic drugs can either suppress the quick-firing pacemaker tissue or depress the transmission of impulses that conduct too rapidly. In patients with atril fibrillation, a blood thinner is usually added to reduce the risk of blood clots and stroke. The effectiveness of antiarrhythmic drugs can be gauged by an electrocardiogram.
Most of the available antiarrhythmic drugs are grouped into four main classes according to Vaughan Williams classification: (I) Sodium Channel Blockers, (II) Beta-Blockers, (III) Potassium Channel Blockers and (IV) Calcium Channel Blockers. In most cases, the drugs have to be taken for the rest of the patient's life.
Class I: Sodium Channel Blockers
Sodium (Na) channel blockers slow conduction in fast-channel tissues by blocking fast sodium channels. These drugs are used for patients with ventricular arrhythmias or recurrent atrial fibrillation. These drugs are typically only used in patients who do not have a structural heart disorder because they may depress ventricular contractility. Some commonly prescribed sodium channel blockers are (generic, brand):
Disopyramide (Norpace)
Flecainide (Tambocor)
Lidocaine (Xylocaine)
Quinidine
Phenytoin (Dilantin)
Class II: Beta-Blockers
Beta-blockers decrease the heart rate and cardiac output, which lowers blood pressure by blocking the effects of adrenaline (what mediates the "fight or flight" response). They affect predominantly slow-channel tissues (SA and AV nodes), where they decrease rate of automaticity, slow conduction velocity and prolong refractoriness. These are used to treat sinus tachycardia, atrial flutter and atrial fibrillation. They are also used to treat chest pain. These are not to be used in patients with asthma. Some commonly prescribed beta-blockers are (generic, brand):
Acebutolol (Sectral)
Atenolol (Tenormin)
Metoprolol (Lopressor)
Nadolol (Corgard)
Propranolol (Inderal)
Class III: Potassium Channel Blockers
Potassium channel blockers prolong action potential duration and refractoriness in slow and fast channel tissues. The conduction velocity is not significantly affected but the capacity for the cardiac tissue to transmit impulses at high frequencies is reduced. These are helpful in patients with atrial flutter, atrial fibrillation and ventricular tachycardias. Some commonly prescribed potassium channel blockers are (generic, brand):
Amiodarone (Pacerone)
Dofetilide (Tikosyn)
Ibutilide (Corvert)
Sotalol (Betapace)
Class IV: Calcium Channel Blockers
Calcium channel blockers slow the heart rate by interrupting the movement of calcium into the heart. These are used to treat high blood pressure, chest pain and arrhythmias. These depress calcium dependent action potentials in slow channel tissues and thus decrease the rate of automaticity, slow conduction velocity and prolong refractoriness. These are especially helpful for patients with atrial fibrillation and supraventricular tachycardia. Some commonly prescribed calcium channel blockers (generic, brand):
Amlodipine (Norvasc)
Diltiazem (Cardizem)
Felodipine (Plendil)
Nifedipine (Procardia)
Verapamil (Covera)
As mentioned above, you can visit www.RateADrug.com to learn about others' experiences with most of the medications listed above. If you would like to let others know about your experience with a particular drug, fill out an anonymous 5 minute survey by clicking on Evaluate This Treatment! I hope you can find something to assist you in your journey with arrhythmia. If you have any questions or comments, please let me know!
Most of the available antiarrhythmic drugs are grouped into four main classes according to Vaughan Williams classification: (I) Sodium Channel Blockers, (II) Beta-Blockers, (III) Potassium Channel Blockers and (IV) Calcium Channel Blockers. In most cases, the drugs have to be taken for the rest of the patient's life.
Class I: Sodium Channel Blockers
Sodium (Na) channel blockers slow conduction in fast-channel tissues by blocking fast sodium channels. These drugs are used for patients with ventricular arrhythmias or recurrent atrial fibrillation. These drugs are typically only used in patients who do not have a structural heart disorder because they may depress ventricular contractility. Some commonly prescribed sodium channel blockers are (generic, brand):
Disopyramide (Norpace)
Flecainide (Tambocor)
Lidocaine (Xylocaine)
Quinidine
Phenytoin (Dilantin)
Class II: Beta-Blockers
Beta-blockers decrease the heart rate and cardiac output, which lowers blood pressure by blocking the effects of adrenaline (what mediates the "fight or flight" response). They affect predominantly slow-channel tissues (SA and AV nodes), where they decrease rate of automaticity, slow conduction velocity and prolong refractoriness. These are used to treat sinus tachycardia, atrial flutter and atrial fibrillation. They are also used to treat chest pain. These are not to be used in patients with asthma. Some commonly prescribed beta-blockers are (generic, brand):
Acebutolol (Sectral)
Atenolol (Tenormin)
Metoprolol (Lopressor)
Nadolol (Corgard)
Propranolol (Inderal)
Class III: Potassium Channel Blockers
Potassium channel blockers prolong action potential duration and refractoriness in slow and fast channel tissues. The conduction velocity is not significantly affected but the capacity for the cardiac tissue to transmit impulses at high frequencies is reduced. These are helpful in patients with atrial flutter, atrial fibrillation and ventricular tachycardias. Some commonly prescribed potassium channel blockers are (generic, brand):
Amiodarone (Pacerone)
Dofetilide (Tikosyn)
Ibutilide (Corvert)
Sotalol (Betapace)
Class IV: Calcium Channel Blockers
Calcium channel blockers slow the heart rate by interrupting the movement of calcium into the heart. These are used to treat high blood pressure, chest pain and arrhythmias. These depress calcium dependent action potentials in slow channel tissues and thus decrease the rate of automaticity, slow conduction velocity and prolong refractoriness. These are especially helpful for patients with atrial fibrillation and supraventricular tachycardia. Some commonly prescribed calcium channel blockers (generic, brand):
Amlodipine (Norvasc)
Diltiazem (Cardizem)
Felodipine (Plendil)
Nifedipine (Procardia)
Verapamil (Covera)
As mentioned above, you can visit www.RateADrug.com to learn about others' experiences with most of the medications listed above. If you would like to let others know about your experience with a particular drug, fill out an anonymous 5 minute survey by clicking on Evaluate This Treatment! I hope you can find something to assist you in your journey with arrhythmia. If you have any questions or comments, please let me know!
Wednesday, June 9, 2010
Existing Nonpharmacological Treatments for Arrhythmia
Conventional treatment modalities include surgery, insertion of medical devices, nonsurgical interventions and pharmacological treatment including medications. Surgical interventions include open-heart maze procedure, ventricular aneurysm surgery and coronary bypass surgery. Medical devices include placement of pacemakers and internal cardioverter defibrillator also known as an ICD. Nonsurgical intervention includes catheter radiofrequency ablation, cardioversion sometimes accompanied with drugs and electrical cardioversion. Pharmacological treatment includes administering antiarrhthymic medications, some of which are listed on this website and will be further discussed in a future post.
Surgery is often only recommended when other options listed above have failed. There are several surgery options available depending on the type of arrhythmia and other complicating factors. The maze procedure is used to treat atril fibrillation. The surgeon directs the heart's electrical activity in the proper order once the cuts have healed. It is called the maze procedure because the electrical impulse can only choose one correct "maze" to travel through. The second surgery, ventricular aneurysm surgery that removes the thinning of the ventricular wall that can be damaged after a heart attack. After a heart attack, the ventricle can become thin, weak and incapable of fully pumping. The third surgical option is a coronary bypass surgery and is usually used for those with serious coronary artery disease. The surgery involves rerouting the blood flow around the clogged artery.
Medical devices such as a pacemaker and ICDs are very common treatments for patients with an irregular heartbeat. For those with bradycardia (slow heartbeat), implantable pacemakers controls the heart's electrical stimulus when the heart's natural pacemaker (sinoatrial node) does not work as it should. The pacemaker can sense that the heart is not beating at the proper time and sends an electrical impulse to make the heart beat. The actual device of the pacemaker consists of a battery to provide power, leads to send the impulse and an electrode to sense each beat of the heart and delivers the electrical impulse when necessary. There are different types of pacemakers dependent on the heart rhythm and therefore vary in the number of leads they contain (one, two or three) and where they are placed (upper or lower chamber). The implantation procedure includes using local anesthesia and receive an additional IV medication for the patient to relax. An ICD or implantable cardioverter defibrillator is a device that acts as a pacemaker for slow heat rate but can also treat fast rhythms. It treats a fast rhythm by delivering the appropriate electrical therapy necessary, whether it be rapid-pacing, low-energy or high-energy shock. Most implantations are done using local anesthesia and possibly a sedative.
The nonsurgical options for treating arrhythmias include radio-frequency ablation and cardioversion. During the radio-frequency ablation, a catheter is placed next to the abnormal pathway and destroys the abnormal tissue. The catheter is inserted into a vein or artery and is commonly used for atrial flutter, supraventricular tachycardias, ventricular tachycardias and atrial fibrillation. The abnormal tissue is destroyed via heat ablation; once the tissue is eliminated, the rapid heart rhythm will be blocked and the rhythm should not occur. This procedure is done under sedation and uses local anesthesia, and may take anywhere from three to seven hours but the recovery time is short. Patients normally return to usual activities within seven days of the procedure. The second option for nonsurgical procedure to treat arrhythmia (particularly atrial flutter and atrial fibrillation) is cardioversion. During this procedure, the patient will be sedated, electrode patches will be placed on the patient's back and chest which are attached to a heart monitor. An electrical impulse will be delivered to the patient's heart through the two large patches to help it return to a normal rhythm. If necessary, multiple impulses will be given to return the heart to a normal rhythm. After the procedure, the patient will only remain in the hospital for a few hours. The only discomfort comes from skin burns on the chest and back where the patches were placed.
As mentioned above, these are just a few of the existing nonpharmacological treatments for irregular heartbeats. Any comments, questions or suggestions are welcome! Coming soon will be the existing pharmacological treatments!! Don't forget to check out www.rateadrug.com to rate drugs that have positively or negatively affected your journey with arrhythmia.
~Alicia
Surgery is often only recommended when other options listed above have failed. There are several surgery options available depending on the type of arrhythmia and other complicating factors. The maze procedure is used to treat atril fibrillation. The surgeon directs the heart's electrical activity in the proper order once the cuts have healed. It is called the maze procedure because the electrical impulse can only choose one correct "maze" to travel through. The second surgery, ventricular aneurysm surgery that removes the thinning of the ventricular wall that can be damaged after a heart attack. After a heart attack, the ventricle can become thin, weak and incapable of fully pumping. The third surgical option is a coronary bypass surgery and is usually used for those with serious coronary artery disease. The surgery involves rerouting the blood flow around the clogged artery.
Medical devices such as a pacemaker and ICDs are very common treatments for patients with an irregular heartbeat. For those with bradycardia (slow heartbeat), implantable pacemakers controls the heart's electrical stimulus when the heart's natural pacemaker (sinoatrial node) does not work as it should. The pacemaker can sense that the heart is not beating at the proper time and sends an electrical impulse to make the heart beat. The actual device of the pacemaker consists of a battery to provide power, leads to send the impulse and an electrode to sense each beat of the heart and delivers the electrical impulse when necessary. There are different types of pacemakers dependent on the heart rhythm and therefore vary in the number of leads they contain (one, two or three) and where they are placed (upper or lower chamber). The implantation procedure includes using local anesthesia and receive an additional IV medication for the patient to relax. An ICD or implantable cardioverter defibrillator is a device that acts as a pacemaker for slow heat rate but can also treat fast rhythms. It treats a fast rhythm by delivering the appropriate electrical therapy necessary, whether it be rapid-pacing, low-energy or high-energy shock. Most implantations are done using local anesthesia and possibly a sedative.
The nonsurgical options for treating arrhythmias include radio-frequency ablation and cardioversion. During the radio-frequency ablation, a catheter is placed next to the abnormal pathway and destroys the abnormal tissue. The catheter is inserted into a vein or artery and is commonly used for atrial flutter, supraventricular tachycardias, ventricular tachycardias and atrial fibrillation. The abnormal tissue is destroyed via heat ablation; once the tissue is eliminated, the rapid heart rhythm will be blocked and the rhythm should not occur. This procedure is done under sedation and uses local anesthesia, and may take anywhere from three to seven hours but the recovery time is short. Patients normally return to usual activities within seven days of the procedure. The second option for nonsurgical procedure to treat arrhythmia (particularly atrial flutter and atrial fibrillation) is cardioversion. During this procedure, the patient will be sedated, electrode patches will be placed on the patient's back and chest which are attached to a heart monitor. An electrical impulse will be delivered to the patient's heart through the two large patches to help it return to a normal rhythm. If necessary, multiple impulses will be given to return the heart to a normal rhythm. After the procedure, the patient will only remain in the hospital for a few hours. The only discomfort comes from skin burns on the chest and back where the patches were placed.
As mentioned above, these are just a few of the existing nonpharmacological treatments for irregular heartbeats. Any comments, questions or suggestions are welcome! Coming soon will be the existing pharmacological treatments!! Don't forget to check out www.rateadrug.com to rate drugs that have positively or negatively affected your journey with arrhythmia.
~Alicia
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