Arrhythmias and drugs Flashcards
define cardiac aryhthmias? what causes it to arise?
abnormal heart rhythm
Arise due to disturbance of impulse generation or impulse conduction or both
what r supraventricular tachycardias?
tachycardias which arises due to problems in the Atria or AV node
what r the actions of of drugs in the CVS?
( what do they alter?)
- rate of rythem
- force of contraction
- Periphersal resistance
- BV
causes of arryhtemias?
explain the phenomenon of “Re-entry”
NOrMALLY>>> electrical impulses reached scarred area in the heart and went around, it but bc electrical conduction is the same in both sides, both impulses reached the end point at the same time and both moved forward. and cancelled out
ok…..
patient with IHD>>>electrical impulse is moving around the dead area, but this dead region has a scarred area! the impulse on one side cannot move forward lana fee block. and on the other side, the impulse will go around noramlly then pass the blocked area. this current will start moving around the dead area over and over again!
if the total time to move around the circle is longer than the time for the block to come out of it refractory period…then the imoulses will start moving around in circles rapidly!= this is called circus movement. it’ll keep on throwing cardiac impulses with every circle to the heart and TACHYARRYHTMEIAS can occur!
Describe the mechanism w/ “triggered activity”
In triggered automacity, after a spontaneoud depolarisation, theres 7alat il triggered depolerization, which can be eithe early or late!
sometimes a new AP is taken off at a very early time> this is called early after depolarization!
or somtimes the RMP is flunctuating causes threshold to be reached faster! causing Delayed after depolarisation
what can cause early after depolarisations?
how would this change on an ECG? on the graph?
if the AP is prolinged
u get longer QT
what can cause delayed after depolarisation?
how would the graph changed?
if the mycoardium cells beomc eischemicor injured, or if they load alot of cations! lots of Ca2+
when more and more r loaded>> causes RMP to flunctuate alot
RMP cannot rest!
Explain the normal Ventricular AP
what r the 4 basic classes of anti-arrhythmic drugs. (in order)
- Drugs that block voltage-sensitive Na+ channels
- Antagonists of β-adrenoreceptors
- Drugs that block K+ channels
- Drugs that block Ca+ channels
other:
Adenosine
antiarrythmetic drugs have the ability to aggravate or cause arrythmeias under certain conditions and must be used with care!
ok
Name Drugs which block voltage-dependant Na+ channels
when do we use them?
anesthetic lidocaine
Sometimes used following MI
– only if patient shows signs of ventricular tachycardia – given intravenously
Name Drugs that r Antagonists of β-adrenoreceptors ?
what r their effects on the heart? What do they do?
when do we use it?
• Slow conduction in AV node
– Can prevent supraventricular tachycardias
– Slows ventricular rate in patients with AF
• After MI
– MI causes increased sympathetic activity
– β-blockers prevent ventricular arrhythmias
– Arrhythmias may be partly due to increased sympathetic activity
• Reduces O2 demand
– Reduces myocardial ischaemia
– Beneficial following MI
how does the slope of the SA node change in the graph when administering a B blocker??
Name drugs that block K+ channels?
what r their effects?
in prolongs the AP, making absolute refractory period longer!
which drug belongs to more than one class?
which drug is used to treat tachycardia associated with Wolff-Parkinson-White syndrome ?
amiodarone
which drug class are not generally used because they can be also be pro-arrythmatic?
Drugs that block K+ channels
Drugs that block Ca2+ channels ? effects?
how will this effect slope of SA node?
Decreases slope of AP at SA node
decrease force of contraction ( - inotropy)
calcium channel blocked,,,snaaaa 3laa bal ma Calcium yirafa3 the slope!
which Ca2+ blockers is not effective in preventing arrhythmias, but do act on vascular smooth muscle
Dihyrdropyridine
name some Ca channel blockers
what r cardiac Glycosides? when do we use it? give example, mechanism of action
Digoxin
more Na will be trapped inside>> causing more Ca to be trapped inside>> Increased force of contraction
which drug is a positive inotrope but will slow conduction at the AV node
Cardiac glycoside
Actions of cardiac glycosides on heart rate
They have a mechanical effect + electrical effect!
- Mechanical = improve contractility of failing heart
- Electrical= prolong refractory time of AV node in patient w/ supraventricular arryhthmias!
– stimulate VAGUS NERVE!> reduces sympathetic activitiy
– slows AV conduction
– slows the HR
what type of drugs increase myocardial contractility ?
β - agonists !
actions of dobutamine? clinical uses?
a synthetic analogue of Dopamine! (acts selectively on B1, but also on B2 and A-recepters)
- to treat reversible HF NOT accompanied with hypotension (cuz it does not increase peripheral resistence bc of the balance bte a-mediated vasoconstriction and B2- mediated vasodialtion)
- cardiogenic shock
Define heart failure
Chronic failure of the heart to provide sufficient CO to meet the body’s requirements
what r u aiming when treating HF?
- Positive inotropes to increase CO (not routinely
- Drugs which reduce work load of the heart – reduce afterload and preload
Drugs used in the treatment of heart failure ?
• Positive inotropes to increase cardiac output (not routinely used)
– cardiac glycosides
– β-agonists
- dobutamine
- Drugs which reduce work load of the heart – reduce afterload and preload
effects of Angiotensin 2?
-
angioTENSIN 2 (gam yisabib tension alaa)
- vasoconstriction
- Stimulates Na reapsorption in kdney>>increase BV
- Stimulates ALDOsterone from arenal cortex
- increases release of ADH from posterior pituatry (translocates aquarporins to allow water retention
ACE inhibitors, clinical uses?
CHRONIC HEART FAILURE
- promotes vasodilation (decreasing preload and afterload)> prevents angie’s vasoconstrictor actions
- diuretic action> lowers BV stops aldosterone release thus Na reabsorption
-
why deos ACE inhbitors cause dry cough?
ACE usually breaks down bradykinin (natural vasodilator)
if u give ACE inhibitors….
Bradykinin accumalates causing dry cough
and acts as a antihypertensive agent!
use __________ if ACEi not tolerated
Ang II receptor blocker
what other drugs can reduce the work load of the heart ? other than Ace inibitors
- β–adrenoceptor antagonists (β-blockers)
- Diuretics
Define Angina?
Angina is chest pain that occurs when the blood supply to the muscles of the heart is restricted (ischemia)
due to narrowing of coronory arterties!
Usually pain with exertion
what r u aiming when treating Angina? (2)
• Reduce the work load of the heart
(this gives more time for the coronory arteries to be filled, rememeber during systole, the heart is compressing on its own blood supply, so we want the ehart to rest shway)
• Improve the blood supply to the heart
how do you treat Angina
• Reduce the work load of the heart
– β-blockers
– Ca2+ channel antagonists
– organic nitrates
• Improve the blood supply to the heart
– organic nitrates
– Ca2+ channel antagonists
mechanism of action of Organic Nitrates?
- NO activates guanylate cyclase
- Increases cGMP
- Lowers intracellular [Ca2+]
- Causes relaxation of vascular smooth muscle
how do nitrates releive symptoms?
WORKS MAINLY ON VEINS!
venodilation>> venous pooling>>less venous return to heart>> less preload
which drug is useful for useful for terminating re-entrant SVT (supraventricular tachycardia)?
Adenosine!
**at high doses nitrates can result in widespread arteriolor dilation>>which can result to systemic hypotension & reflex tachycardia!
ok
Why do organic nitrates preferentially act on veins?
- Probably because there is less endogenous NO in veins
- Most effective on veins > arteries
- Little effect on arterioles
what r some classes of Antithrombotic drugs
- anticoagulants
- Antiplatelets
give examples of anticoagulant drugs and what they target?
- heparin (IV) >>inhibits thrombin
- Fractioned Heparin (subcutaneous ibra)
- warfarin (orally)>> antagonizes action of VK
- direct acting oral thrombin inhibitors> diagbatran
the newer one (last one) is effective bc u dont have to do the regular blood tests that u would do with warfarin
give examples of antiplatelet drugs and what they target?
Aspirin
blocks cyclooxygenase in platelets
(which normally converts AA to TXA2)
bc platelets lack nuclei and cannot synthesize new proteins, aspirin permentantly disables TXA2
Treatment of Hypertension ?
• ACE-inhibitors
– decrease Na+ and water retention by kidney
– decrease total peripheral resistance - vasodilation
• Ca2+ channel blockers
selective for vascular smooth muscle – vasodilation
• Diuretics
– decrease Na+ and water retention by kidney
• decrease BV
• β-blockers (not routinely used)
– decreases CO
• α1 – antagonist (not routinely used)
– vasodilation
what is adenosine?
ideeeeloooooooo aywa aywa! rag9! rag9!>> sawanyy hyperrrr
- Acts on A1 receptors at AV node
- administered IV
- but has a very short half-life 15 sec!
- increases K+ out of cells>> causes hyperpolarisation
- (this inhibits spontaneous depolarization of the SA node, and slows conduction throught he AV node, it aslo supresses CAMP byinhibiting aDenylyl cyclase)
Antoiar
Explain how tachycardia can reduce cardiac output.
Not enough time for ventricles to fill,
Reduced stroke volume
How can long-standing mitral valve stenosis precipitate atrial fibrillation?
Increased pressure in left atria
Stretches the atria
A patient is in intensive care following a myocardial infarction. The intensive care nurse notices that his heart rate has gone into ventricular tachycardia. What is the risk with this rhythm?
Risk of ventricular fibrillation
Amiodarone is now more often used than lidocaine in an
emergency setting to treat ventricular tachycardia or VF because itis more effective.
How does amiodarone work?
Amiodarone is an important antiarrhythmic agent which acts on Na+, K+ and Ca2+ channels as well as β- adrenoceptors.
What will happen to the concentration of Na+ inside the cells if the Na+/K+ pump in the membrane is partially inhibited by a drug such as digoxin?
increases
Why do you give adrenaline intravenously to someone whose heart has stopped (i.e. in ‘cardiac arrest’)?
Circulating adrenaline activates B2 adrenoreceptors on bv which causes vasodilation at high concentrations.
At high concentrations, it binds to A1 which causes vasoconstriction and leads to increased preload
Binds to B1 adrenoreceptors to increase force of contraction + heart rate
What would be the action of a ß adrenoreceptor antagonist on an individual with an abnormal increase in heart rate arising above the level of the ventricles (i.e. a supra-ventricular tachycardia SVT due to AV nodal re-entry)
B- adrenoreceptor antagonist would decrease HR and inotropy
Decrease slope of pacemaker potential in SA
Slows conduction at AV node - prevents supraventricular tachycardias, slows ventricular rate in patients wth AF
What might be the effect of atropine upon an individual with an abnormally low heart rate (‘bradycardia’)?
Antimuscarinic -
Decrease parasympathetic input to the heart via vagus nerve Increases heart rate
Why are individuals whose coronary blood flow is compromised, treated with ß adrenoreceptor antagonists? What effect do these drugs have on the force of contraction of the heart, heart rate and oxygen demand of the myocardium
Beta adrenoreceptor antagonists
- Force of contraction of heart - decrease
- Heart rate - decreases.
- oxygen demand -decrease
Describe the main mechanism by which organic nitrates relieve the symptoms of angina.
Reactions of organic nitrates with thiols causes NO2- to be released NO is a powerful vasodilator
Venous relaxation which decreases preload
Dilates collateral arteries so that blood can flow to the ischaemic area
What would normally be the most appropriate drug to give a patient suffering from chronic heart failure, but with no arrhythmia,
ACE inhibitor - decrease the workload of the heart without decreasing heart rate
