[PBS 8] Midterms

fibrilation

350 above

flutter

250-350

paroxysmal tachycarida

150-250

simple tachycardia

100-150

normal

60-100

mild bradycardia

40-60

moderate bradycardia

20-40

severe bradycardia

20 below

purkinje system

• Gives electrical impulses in cardiac tissues

• Reason why ventricles are thicker

non-pacemaker cells

• Do not initiate action potential

• Atria, ventricles, purkinje system

  • Only receive action potential that SA node gives

• Divided into 4 phases

phase 4 NP

• Flat line

• Cell at rest

• Charge = negative

• Potassium outwards

  • Towards conc. gradient

• 90 mv ususal charge

phase 0 NP

• Action potential shoot up

• Sodium inside

• Sodium channel = open Depolarization

phase 1 NP

• Repolarization starts

• Sodium closes

• Potassium opens

• Quick phase

phase 2 NP

• Plateau

• Isoelectric

• Potassium exits (close)

• Calcium enters (open)

• Net charge = o

phase 3 NP

• Repolarization

• Calcium channel opens

• Potassium open

• Mas marami cations nalabas

• Decrease positivity = repo Sodium opens out

pacemaker cells

• SA node mas batas

• AV node pag sumuko SA

• Nodal arrhythimia = pag di sumunod

• Has unstable resting membrane potential

• If it rests = blockade

  • Therefore IT DOES NOT REST

• No phase 1 = no fast repolarization

• No isoelectricity = no balance

phase 4

Slightly depolarized due to automacity

phase 3

• Repo to hyper

• Potassium will open

• Calcium will close

electrocardiogram

• Holds the record of cardiac beat (heart beats)

• Segment

  • Flat = isoelectric

  • Ventricles = still depolarized

p wave

• Atrial depolarization

• Atrium = action potential

• Atrium = contracts

• Lipat blood from atrium to ventricle

PR interval

• Beginning of P wave to Q wave

• Time consumed AP from SA to AV

• Dromotropy

• If short (positive dromotropy)

• Fast mass of action potential

• If long (normal, negative dromotropy)

  • Slow transfer

  • Long enough to fill blood

  • Can be prolonged through parasympathetic

QRS complex

• Beginning of Q wave until S wave

• Ventricular depolarization (contraction)

• Blood goes systemic

ST segment

• End of S wave until beginning of T wave

• Isoelectric (phase 2)

• Ventricles are still depolarized

T wave

• Ventricular repolarization

• Ventricular relaxation

QT interval

• QRS complex until end of T wave

• Time of contraction and relaxation of ventricle

conduction velocity

• Reflects the time required for excitation to spread throughout cardiac tissue

• Depends on the size of the inward current during the upstroke of the action potential

  • The larger the inward current, the higher the conduction velocity

• Is fastest in the Purkinje system

• Is slowest in the AV node

• SA = Calcium

• AV = Sodium

excitability

• Ability of cardiac cells to initiate action potentials in response to inward, depolarizing current

• Reflects the recovery of channels that carry the inward currents for the upstroke of the action potential

• Changes over the course of the action potential

  • These changes in excitability are described by refractory periods · ERP = Effective Refractory Period

• Phase 0-3

• If potassium blocked = longer repolarization ·

• If sodium channel blocked = faster repolarization

• ERP should finish before next ERP

arrhythmia

• Heart condition where there are disturbances or disorders in

• Pacemaker impulse formation § SA node = no electrical impulse in heart § ↓ CO = ↓ O2 complications

• Contraction impulse conduction

• Both

• Result in rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output

Ectopic pacemaker

• Outside (AV node sasalba), purkinje fibers

automacity

• Ability of certain cells of the heart (non-pacemakers) to undergo spontaneous depolarization, in which an action potential is generated without any influence from the nearby cells

enhanced automaticity

• increase in slope of phase 4

• Fast repolarization

triggered automaticity

• second depolarization occurs prematurely

• EADs § DADs

Arising From The Sinus Node

• Sinus tachycardia (100-150 bpm)

• Sinus bradycardia (<60 bpm)

Atrial Arrhythmia

• Atrial fibrillation (around 350bpm)

• Atrial flutter (250-350bpm)

Nodal And Other Supraventricular Arrhythmias

• Atrioventricular block (Prolongation of PR interval)

• SA AV

• Impulse prolonged = blocked

Supraventricular Tachycardia

• Intranodal SVT (Re-entry 'circus' tachycardia)

• Extranodal SVT

• Wolff-Parkinson-White Syndrome § Lown-Ganong-Levine Syndrome

extranodal svt

• Wolff-Parkinson-White Syndrome

• Lown-Ganong-Levine Syndrome

• Ventricular Arrhythmias

ventricular arrhythmias

• Ventricular Ectopic Beats (outside)

  • Abnormal QRS Complex (ventricular contraction)

• Ventricular Tachycardia

  • Rapid, wide QRS complex

• Ventricular Fibrillation

  • Chaotic; circulatory arrest occurs immediately

ventricular ectopic beats

Abnormal QRS Complex (ventricular contraction)

ventricular tachycardia

Rapid, wide QRS complex

ventricular fibrilation

Chaotic; circulatory arrest occurs immediately

suppress automaticity

• Decrease the frequency of discharge, an effect that is more pronounced in cells with ectopic pacemaker activity than in normal cells

• By decreasing the slope of phase 4 (diastolic) depolarization

• By raising the threshold of discharge to a less negative voltage

prevent re-entry

• By converting a unidirectional block into a bidirectional block

• Slow conduction

• Increase the refractory period

sodium channels

• Inhibit re-entry

• Inhibit automaticity (triggered, enhanced)

• Decrease depolarization

blockade of sympathetic autonomic effects

• Inhibit re-entry but NOT automaticity

• Cause prolongation of QRS = ventricles

prolongation of effective refractive period

• Longer blocking

• Potassium channel blockers

calcium channel blockade

• C2 and C3

• Cannot block automaticity

miscellaneous

• Adenosine

• Digitalis glycosides

• Magnesium ions

• Potassium ions

quinidine procainamide disopyramide

class 1a

tocainide mexiletine lidocaine phenytoin

class 1b

moricizine flecainide propafenone encainide

class 1c

propranolol atenolol

class 2

amiodarone bretylium ibutilide sotalol

class 3

verapamil

class 4

adenosine digitalis

miscellaneous

class 1 fast sodium

• Block the fast inward sodium current · Sometimes termed "PVC killers"

• Premature Ventricular Contraction

• Depress the rate of spontaneous phase 4 depolarization, or automaticity

• Useful for abolishing premature ventricular contractions

• Depress Phase 0

• Shoot up

• Indirect w/ phase 0

• Bumaba = sodium, can target AUTOMATICITY

class 1a

• Cause moderate phase 0 depression

• Prolong repolarization (non-specific blockade of potassium channels)

• Prolong the APD and dissociate from the channel with intermediate kinetics

• Increases ERP

• Depress and prolong ERP

quinidine

• First antiarrhythmic used

• Slows the upstroke of the action potential and conduction, and prolongs QRS duration of the ECG

• Treats both atrial and ventricular arrhythmias (anticholinergic effect)

• Used for digitalis-induced arrhythmias o antidote

• Cinchona bark

• Prototype

• Depress phase 0

• Inhibits muscarinic

toxic effects of quinidine

• Excessive QT interval prolongation and induction of torsades de pointes arrhythmia

  • ↓ QT interval = ↓ QRS

• Diarrhea, nausea and vomiting (muscarinic)

• Cinchonism

  • Headache, tinnitus, dizziness

• Idiosyncratic or immunologic reactions, including thrombocytopenia, hepatitis, angioneurotic edema and fever (rare)

• Can cause arrhythmia

cinchonism

• Headache, tinnitus, dizziness

torsades de pointes

• Uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of QRS complexes around the isoelectric line

• Excessive prolongation

procainamide

• Direct depressant actions on sinoatrial and atrioventricular nodes

• Can suppress automaticity

• Less anticholinergic effects than quinidine (less basa)

  • Effective against most atrial and ventricular arrhythmias

• Drug of second or third choice for sustained ventricular tachycardia associated with acute MI

toxic effects of procainamide

• QT interval prolongation, and induction of torsades de pointes arrhythmia

• Syncope

• Syndrome of lupus erythematosus

• Nausea and diarrhea, rash, fever, hepatitis, and agranulocytosis

disopyramide

• Effective in a variety of supraventricular arrhythmias

• Extended duration of action, used only for treating ventricular arrhythmias

• Anticholinergic effects are even more marked than that of quinidine

• Accounts for most adverse effects

atropine like effects

• Dry mouth (Xerostomia)

• Urinary retention (xxx for BPH px)

• Blurred vision

• Constipation

class 1b

• Weak phase 0 depression

• Shortened depolarization

• Decreased action potential duration

• ERP is diminished

lidocaine

• Also acts as a local anesthetic

• Blocks sodium channels mostly in ventricular cells, also good for digitalis-associated arrhythmias (suspect drug)

• Not a depressant of AV node (shortened ERF)

• Agent of choice for ventricular tachycardia and prevention of ventricular fibrillation (Given as IV to bypass FPE)

• First line for digoxin induced

toxic effects of lidocaine

• Least cardiotoxic

• Neurologic

  • Paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech and convulsions

mexiletine

• Oral lidocaine derivative, similar activity as lidocaine

• Used in the treatment of ventricular arrhythmias

phenytoin

• Anticonvulsant that also works as antiarrhythmic similar to lidocaine

class 1c

• Strong phase 0 depression

• No effect on action potential duration

• Does not block potassium kaya no change in phase 3

• Does not shorten ERP, only delays depolarization Huge time difference

flecainide

• A potent blocker of sodium and potassium channels

• Slows conduction in all parts of heart

• Very effective in suppressing premature ventricular contractions

• May cause severe exacerbation of arrhythmia even when normal doses are administered

  • Patients with preexisting ventricular tachyarrhytmias

  • With a previous myocardial infarction and ventricular ectopy

• Insignificant action in repolarization

propafenone

• Weak beta-blocker

• Also some calcium channel blockade

• Spectrum of action is the same with quinidine (↓ contraction)

• Used primarily for supraventricular arrhythmias

• Resembles propranolol

• ↓ HR

• Proarrhythmic drug

  • Irresponsible use = arrhythmia

• Only ABOVE

adverse effects of propafenone

• Metallic taste and constipation

• Arrhythmia exacerbation

moricizine

• A phenothiazine derivative that was used for the treatment of ventricular arrhythmias (antipsychotic)

• Has been withdrawn from the US market

• Only BELOW

class 2

• Based on two major actions:

• Blockade of myocardial beta-adrenergic receptors

• Direct membrane-stabilizing effects related to sodium channel blockade

• Re-entry

propranolol

• Causes both myocardial beta-adrenergic blockade and membrane stabilizing effects

• Slows SA node and ectopic pacemaking

• Can block arrhythmias induced by exercise or apprehension

• Prototype that possesses MSA

esmolol

• Short-acting

• Used in intraoperative and other acute arrhythmias T1/2 = 10 mins

sotalol

• Racemic mixture

• L type = beta blocking

• D type = prolong AP, increase ERP

class 3

• Prolong action potentials

• Developed because some patients are negatively sensitive to sodium channel blockers

• Cause delay in repolarization and prolonged refractory period

  • Time to phase 0 to the end of phase 3 of the action potential

• Unaffected depolarization

• No changes for phase 0

amiodarone

Prolongs action potential by delaying potassium efflux

ibutilide

Slows inward movement of sodium channel in addition to delaying potassium efflux

bretylium

Has no effect on either automaticity or conduction velocity

It blocks the release of norepinephrine

dofetilide

Prolongs action potential by delaying potassium efflux with no other effects

amiodarone

• Also blocks inactivated sodium channel

• Has weak adrenergic and calcium channel blocking actions

• Slowing of the heart rate and atrioventricular node conduction

• Has a broad spectrum of actions

• High efficacy

• Low incidence of torsades de pointes

• Causes peripheral vasodilation (IV)

• 1st line for ventricular tachycardia (any origin)

• ↓ AV = ↑ efficacy

toxic effects of amiodarone

• Bradycardia and heart block in patients with preexisting sinus or AV node disease

• Fatal pulmonary fibrosis (1%)

• Most serious (scarring in lungs)

• Hepatitis and abnormal liver function

• Skin deposits (photodermatitis)

• Corneal microdeposits

• Halos on the peripheral visual fields

• Optic neuritis (rare)

• Hypothyroidism or hyperthyroidism

• Blocks the peripheral conversion of thyroxine (T4) to triiodothyronine (T3)

• Can alter thyroid hormone

• Can increase iodine

  • 32% of its weight

• Phase 1 = hypo

• Phase 2 = hyper

• Wolf-chaikuff effect

fatal pulmonary fibrosis

• Most serious (scarring in lungs)

corneal microdeposits

• Halos on the peripheral visual fields

• Optic neuritis (rare)

dronedrone

• Similar effects as amiodarone

• No thyroid or pulmonary toxicity

• Structurally similar

• No iodine content

vernakalant

• An investigational multi-channel blocker that was developed for the treatment of atrial fibrillation

• Adverse effects include

• Dysgeusia (disturbance of taste)

• Sneezing

• Paresthesia

• Cough

• Hypotension*

• Clinical trial

dofetilide

• Approved for the maintenance of normal sinus rhythm in patients with atrial fibrillation

• Also effective in restoring normal sinus rhythm in patients with atrial fibrillation

ibutilide

• Used for the acute conversion of atrial flutter and atrial fibrillation to normal sinus rhythm

• Adverse effect is excessive QT interval prolongation and torsades de pointes

• Slow depolarization

bretylium

• First developed to treat hypertension but found to also suppress ventricular fibrillation associated with myocardial infarction Blocks exocytosis

class 4

• Slow rate of AV-conduction in patients with atrial fibrillation

verapamil

• Blocks sodium channels in addition to calcium channel

• Also slows SA node in tachycardia (automaticity)

• Constipation

• First line for Chronic PVST

diltiazem

• Has actions for blood vessels xxx

digoxin

• increases vagal activity (parasympa) via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node and increases the refractory period

• Dose dependent

  • Low dose = negative chronotropy

  • High dose = tachycardia · Narrow TI

toxic effects of digoxin

• May produce an increased automaticity characterized by multifocal premature ventricular depolarizations

• Caution must be observed in digitalizing a patient who is prone to atrial dysrhythmias, because digitalis increases atrial excitability and hence increases the risk of atrial ectopy

• Always monitor

smooth vascular muscle

• Adenosine binds to adenosine type 2A (A2A) receptors, which are coupled to the Gs protein leading to an increase in the cAMP

• Stimulates KATP channels, which hyperpolarizes the smooth muscle, causing relaxation

• Causes smooth muscle relaxation by inhibiting myosin light chain kinase, which leads to decrease myosin phosphorylation and a decrease in contractile force

effect on cardiac tissues

• Adenosine binds to type 1 (A1) receptors which are coupled to Gi-proteins leading to decrease cAMP, causing inhibition of L-type calcium channels

• Inhibits the pacemaker current - negative chronotropy

• Decreases conduction velocity (negative dromotropic effect) particularly at the AV nodes · Blocks NE = block exocytosis

• ↓ chronotropy, ↓ dromotropy