Pharmacology Flashcards
(23 cards)
Why does dysrhythmia need treated?
Degeneration can lead to a fatal rhythm and have impacts on the cardiac output especially if long term
The cardiac muscle has a stable resting potential, what is this determined by?
Determined by potassium concentrations
Explain how the cardiac muscle is depolarised and then repolarised:
4 stages
1 = Depolarising - sodium permeability increases allowing an influx in sodium ions depolarising the cell and reaching actin potential
2 = Maintaining - voltage gated calcium ion channels switch between open and closed allowing a slow influx maintaining depolarisation
3 = Repolarising - calcium and sodium channels close on potassium channels open
4 = cell reset and waiting for next impulse
Why is cardiac muscle action potential much longer than other neurones?
Cardiac action potential is mainly mediated by voltage gated calcium channels instead of sodium like the others.
The calcium channels open and close gradually and so the action potential builds up over a long period of time instead of rapid fire.
Action potential plus pacemaker potential is the …..
Absolute refractory period
Describe what goes on in a pacemaker cell for it to randomly depolarise?
3 stages (0, 3, 4)
0 = Depolarisation - voltage gated calcium channels open allowing an influx and reaching action potential
3 = Repolarisation - calcium channels close and voltage gated potassium channels open
4 = Slow depolarisation - potassium channels close and sodium and calcium channels spontaneously open allowing a slow influx until -40 (this is unique to pacemaker cells)
cycle begins again!
What determines HR in the pacemaker cell?
How long the stage of slow depolarisation is
What increases calcium movement in cells?
What impact does more calcium have on contraction force of the heart?
What impact does and increase in calcium have on HR?
The sympathetic nervous system, more nor-epinephrine means more calcium movement
Increases in calcium is important as plays a large role with actin and myosin cross bridges and therefore muscle contraction force
Increase in calcium increases heart rate as calcium plays a role in muscle and pace maker cells and the calcium in now moving faster
Muscle cells - decreased plateau phase
Pacemaker - calcium channels open quicker so action potential reached faster and reset quicker
What causes dysrhythmia?
- congenital, developmental or trauma structural cardiac disease (changes shape, size of muscle changing movement of electrical system)
- drugs and toxins (can change sympathetic system etc.)
- metabolic diseases/electrolyte imbalance (such as potassium or calcium e.g. renal disease)
- systemic disease (sepsis, neoplasia)
- sympathetic tone (increased epinephrine release e.g. pain, fear)
How can you treat dysrhythmias?
- treat underlying problem
- agonist/antagonist on receptors
- drugs affecting ion channels (not via receptor)
What drug can be used to block the sympathetic nervous system if it’s gone a bit too far and heart rate is too high and the heart can no longer fill properly? (supraventricular tachycardia)
What are 2 examples of these types of drugs?
Beta blockers, agonists that block the beta 1 and 2 receptors
Propranolol
Atenolol
How do drugs that slow down heart rate by acting like the parasympathetic system work?
ACh binds to muscarinic receptors which blocks adenylyl cyclase, reduces cyclic amp and reduces calcium uptake (which then impacts calcium release). It also opens the potassium channels on the other side allowing potassium to leave the cell, taking the baseline of -65 even lower as it removes the + ions without replacing hyperpolarising the membrane making it harder to reach depolarisation threshold slowing down heart rate and reducing contraction.
How do muscarinic antagonists work?
What is an example?
They block the muscarinic receptors preventing hyperolarisation and down regulation of cyclic AMP reversing effects of muscarinic receptors and the parasympathetic NS, HR and contraction force should increase. (an example would be used for patients with severe brachycardia)
Atropine
What is parasympathetic/vagal tone?
Being chronically unwell
Can also be caused by severe abdominal pain
It causes your HR and contraction force decrease
What do muscarinic agonists do?
What is an example of a drug that does this?
They bind to the muscarinic receptors and mimic acetyl choline by blocking adenylyl cyclase and reducing cAMP and calcium effects whilst hyper polarising the cell slowing the heart rate and contraction force.
Muscarine found in mushrooms
Muscarinic agonists ..1… the parasympathetic nervous system
Muscarinic antagonists ..2… the PSNS
In using these what are you trying to achieve?
- activates/mimics
- blocks/suppresses
Trying to get the heart rate back to the normal baseline
What is adenosine?
When would you use adenosine?
Drug that acts on a specific receptor (like an agonist) in the heart that acts like a muscarinic receptor: blocking cyclic amp, increasing potassium reflux, slowing down calcium manipulation
Resulting in a fast drop in heart rate and contraction force.
In emergencies on severe tachycardia patients as short acting and very fast, not pleasant for patient
What do sodium channel blockers do?
Which is most commonly used in practice?
Why are they often used as local anaesthetics?
Slows down action potential as impacts the depolarisation phase, also slows the heart as it also has an effect on those sodium channels
Lidocaine
Reduces action potential movement as these cause the feeling of pain as they pass the signal from the pain stimulus to the brain
What type of drugs are needed when dealing with ventricular tachycardia?
Must be drugs acting on the ion receptors. Drugs that act on the PSNS and the SNS won’t work as it has nothing to do with the sinoatrial node. It is the ventricular muscle not working on its own accord.
How do potassium channel blockers work?
When would you use potassium channel blockers?
Give two examples of potassium channel blocker:
Block the potassium channels slowing down depolarisation which means it takes longer for the cells to reset themsevm for the next wave of depolarisation. So they slow down heart rate and contraction force.
If the sodium channels blockers, like lidocaine weren’t working or in an emergency or for longer term treatments.
- Amiodarone (short acting, emergency use like CPR)
- Sotalol (longer acting, if you had a damaged myocardium that was causing ventricular tachycardia while it healed something like this can be a longer acting treatment for a few weeks until it sorts itself)
What are the 3 types of ion channel blockers?
Calcium
Sodium
Potassium
When would calcium channel blockers be used and why?
Are they really used for the heart?
To slow conduction, reduce contraction force and cause coronary vasodilation as calcium influx will slow prolonging the plateau [hase and less calcium will be released from the sarcoplasmic reticulum as calcium induces calcium release.
No, more preferred for reducing blood pressure
What is the name of the drug that inhibits the potassium sodium pump and what effect does this have on the heart?
Why is it so dangerous?
Digoxin - increases the atrioventricular refractory period slowing down the heart and improves filling. It also causes the cell to maintain calcium as it changes its movement across the membrane which increases contraction force.
Very fine line when working with, can easily kill the patient and can have an effect on any pump in any part of the body so any there drugs that have side effects that could react with the pump will then react badly with the digoxin
