#cardiac
My latest heart.
I know - another heart. I still love making them and, at this time of year, I get a lot of requests. Each is unique - sometimes on purpose, sometimes to cover up an accident - drill scratch, hole in the wrong place etc. The heart itself is vintage - new old stock from the 1970s - a lucite core with a thick copper plate. They are still available but, eventually, I’ll have to find an alternative. I’d love to find similar wood hearts - that could be hinged with a secret internal compartment. If anyone knows where something like that can be sourced - let me know. Dimensions would be 1 ½ inches wide/high and about ¾ of an inch deep so they could be cut and hollowed out.
The next one I’ll be making will be a bit different - a central “window” with a flashing red LED - with batteries that can be replaced. It will have to be a symmetrical design with a feature taking up that much real estate on the heart. I’m starting it tonight and I’ll post a video of it to show the “flash”.
In order to better understand cardiac defects, it’s best to start off reviewing how a normal heart works. First, the Superior and Inferior Vena Cava carrydeoxygenated blood into the heart (Right Atrium) from other parts of the body. The deoxygenated blood then passes through the TricuspidValve into the Right Ventricle. Thedeoxygenated blood is following the pathway through the heart in order to get to the lungs to gain oxygen, next the blood passes through the PulmonaryValveand enters the Pulmonary Artery, the pulmonary artery is special because it is the only artery in the body that carries deoxygenated blood. Once the deoxygenated blood passes through to theLungsit becomes oxygenated. The newly oxygenated blood then flows back to the heart through the Pulmonary Veins and into the Left Atrium. It then passes through the MitralValveand into the Left Ventricle. The blood is then contracted through the AorticValveinto the Aortaand to the rest of the body.
The Fetal Heart:
During the fetal period and some time after birth, the circulation is quite different. The heart has more, holes, if you will in order for the fetal blood to bypass the lungs that are unable to oxygenate blood while the fetus is in utero.
- The Foramen Ovale is an opening that allows passage of blood from the Right Atrium directly into the Left Atrium. The blood passing through is already oxygenated from the placenta.
- The Ductus Arteriosus is an opening that passes oxygenated blood from the Pulmonary Artery directly into the Aortato get pumped to the rest of the body.
Normal changes in the heart after birth:
- Ductus Arteriosus closes
- Foramen Ovale closes
- Ductus Venosus (connection from the umbilical cord) closes
There is quite a lot to be said about the medications we use for patients with arrhythmias. It’s easy to get lost as to what drugs do what and how, but thankfully there was a kind enough person by the name of Vaughan Williams, who actually broke them down into separate classes. Each class effects separate parts of the cardiac cycle, ultimately changing the electrical current of the heart.
Cardiac Action Potential
Before looking at the medications, we have to understand the cardiac cycle and how it actually works.
Source:x
The above chart presents the four phases of an action potential in a ventricular myocardial cell and how the electrolytes are used to cause the depolarization and repolarization of myocardial cells.
Phase 0 begins with a slight influx of sodium until it passes the potential threshold. Once past the threshold, more sodium channels will open and flood the cell, causing it the depolarize.
Phase 1 is an efflux of potassium from the cell, causing the cell to reach 0mV.
Phase 2 happens at this point. This is when calcium influx happens, prolonging the repolarization period. This period also goes by the name of an absolute refractory period for the cell, since it cannot depolarize during this time.
Phase 3 Calcium channels close again and potassium continues to efflux from the myocardial cell until the internal cell voltage returns to -90mV. Majority of potassium channels then close and the heart enters phase 4, which potassium is allowed to continue to leak into from the cell.
This process happens anywhere from 60 to 100 times per MINUTE!
Vaughan Williams Classifications
The major purpose of the medications in this class effect they way the cardiac action potential works in the cells of the heart. The drugs usually help to slow down specific phase to the heart and allow the heart to fix itself a bit.
Class I - Sodium Channel Blockers
These medications are designed to disrupt phase 0, causing a prolongation of it. There are 3 subcategories (a,b,c) that are broken down into moderate, weak, and strong.
This article won’t go into great depths, but the major goal of the class is to prolong the QRS complex and prolong or shorten QTi.
Medications include:
Lidocaine
Verapamil
Procainamide
Propafenone
Class II - Beta Blockers (-olol or -alol)
Quite commonly used out of hospital for patients with hypertension, beta blockers are actually a common antidysrhythmic. The basic pharmacology is: by blocking the beta-1 receptor sites, it prevents stimulation of the cardiac muscle to beat faster. The increase of sympathetic tone will decrease the rate the heart will beat.
Medications include:
- Propranolol
- Metoprolol
- Carvedilol
Class III - Potassium Channel Blockers
Similar to the Class Ia medications, potassium channel blockers are used to prolong APD, which can cause a prolongation of ERP. This class of medication is commonly known to treat different ventricular dysrhythmias (Vtach or Vfib). The most common medication for this class is Amiodarone and deserves a post of its own.
It’s most common use is during CPR, when the patient is in pulses Vtach or Vfib rhythm and is then followed by a drip with ROSC is achieved. An important note to make about Amiodarone is it can take 16 weeks to leave the system.
Medications include:
- Amiodarone
- Sotalol
- Ibutilide
Class IV - Calcium Channel Blockers
Commonly uses for Afib with RVR and PSVT, a calcium channel blocker will prolong phase 2 of the action potion in the cell. The goal is to slow the conduction through the atrioventricular (AV) node, slowing the ventricular tachycardia that is occurring. By prolonging the ERP in the AV node, the heart is able to regulate the rate better.
Calcium channel blockers are commonly prescribed by physicians to assist in the care of such arrhythmias. One side effect of these drugs is it may drop the patient’s BP, so ensure you have an SBP >100 or a MAP >65, prior to administering the medication
Class V - Others
This is the mix bag class. These drugs do not truly fit in any category but are still highly important to mention anyways. Two of these medications are Adenosine and Digoxin.
Adenosineprevents the re-entry of a signal in a sinus rhythm, preventing SVT. A warning though is for patients that have WPW syndrome may cause an increase in heart rate instead, so make sure you’re reading the rhythm correctly.
Digoxineffects vagal tone and is seen less as an emergency drug and more as a maintenance drug for chronic heart issues. A major issue with this drug is it holds a very narrow therapeutic index. Toxicity is quite possible if given too much.
Summary
Each class works in its own way on the action potential in the cardiac conduction system. How they affect the heart greatly determines when and how the medication should be used in different medical scenarios. The point of this article is to help a bit with the pharmacodynamics involved with the medications and to hint at the situations a person in the medical field would use them?
Remember to check out my facebook page. Feel free to send suggestions for possible article ideas, it might pop up some time. Always remember that medicine is an art, just as much as a science.