CLASS 22 - Cardiac Arrhythmias + Exemplars Flashcards
What does it mean to be chronotropic ?
Affects the heart rate and rhythm by affecting the electrical conduction system of the heart
What does it mean to be inotropic?
Changes the force of the heart’s contractions. Can be +ve or -ve inotropes.
Positive inotropes strengthen the force of the heartbeat, negative inotropes weaken the force of the heartbeat.
What initiates the Cardiac Conduction System?
The SA node.
Why is the SA node considered to be the pacemaker of the heart?
the cells of the SA node spontaneously depolarize FASTER than other cardiac cells and create electrical impulses, therefore setting the normal rhythm and rate of the heart.
once the SA node creates an electrical impulse, where does it travel?
travels through atria and reaches the AV node.
then travels to the ventricles by the bundle of His and the Purkinje fibers
synchronized so that all ventricles contract at the same time
what is overdrive suppression?
SA node depolarizes first and resets all other cells
what is an ectopic rhythm?
occurs if another cardiac cell initates contraction resulting in premature atrial conraction
describe the effects of the SNS and PSNS on the SA Rate
SNS: increases SA rate
PSNS: slows SA rate via vagus nerve
what is the only electrical pathway from the atra to the ventricles?
AV node
what is the PR interval?
AV node conduction
what is a normal sinus rhythm (NSR)?
temr used to decribe a normal ECG rate and rhythm generated in the SA node
what are the effects of potassium balances on the ECG?
potassium has effects on the myocardium’s resting potential and ability to repolarize
potassium imbalances tend to slow impulse conduction through the AV node and myocytes.
what are the effects of hypokalemia on the ECG?
- PR
- ST
- U
- QT
prolonged PR depressed ST low or inverted T appearance of U increased in QT
what are the effects of hyperkalemia on the ECG?
diminished or absent P
widening of QRS
peaked T
unexcitable cells
progresses to VT or VF and cardiac arrest
what are ‘U’ waves thought to represent?
repolarization of purkinje fibers
compare cardiac arrhythmias and dysrhythmias
arrhythmias are alterations in cardiac rhythm, where dysrhythmias imply loss of rhythm
when are cardiac arrhythmias / dysrhythmias harmful?
when the interfere with the heart’s pumping ability.
what do cardiac arrhythmias / dysrhythmias indicate ?
may indicate alterations in automaticity, excitability, conductivity, or refraction due to ischemia and infarction, electrolyte imbalances, drug effects, or defects in condiction.
what is sinus bradycardia?
where is it often seen?
defined as sinus rhythm with a resting rate less than 60 per minute
seen in trained athletes or during sleep, but may occur during myocardial infarction, respiratory depression, hypothyroidism, or drug toxicity.
can also be a compensation for an underlying disorder.
what is sinus tachycardia?
sinus rhythm with a resting rate over 100 per minute
seen with exercise or fever, but may occur with CHF, MI, hyperthyroidims, drug toxicity, and hypovolemia
why are sinus tachy - and bradycardia not often treated directly?
bc they usually occur secondary or as a compensation for another underlying disorder.
describe increased automaticity as a mechanism of arrhythmias.
increase in the natural depolarization rate of nodal cells
occurs commonly in response to SNS activation, can lead to uncontrolled electrical activity
decribe triggered activity as a mechanism of arrhythmias
occurs whn ischemia or fibrosis are present, or during heart failure.
following a normal AP, myocytes can sometimes depolarize spontaneously. These are called early or delayed afterpolarizations. (EAD or DAD) commonly causes ectopic or premature beats.
how does re-entrant activation occur?
in the presence of a one-way block, the stip of muscle is excited at only one location (instead of 2)
impulses spreading from this area meet no impulses coming from the left, and therefore can trael far enough to simulate branch 1 of the Purkinje fiber . This stimulation passes back up the fiber, past the region of one-way block, and then stimulates branch 2, causing reentrant activation.
what are premature atrial contractions (PAC)?
Premature atrial beats that originate within the atria but outside of the sinus node (ectopic beat)
what are the potential causes of PACs?
stimulants such as tobacco, emotion, or coffee
hypoxia/ischemia, electrolyte imbalances, or other cardiac conditions
what are the key ECG features of Premature Atrial Contractions?
underlying NSR
P-P interval shortened on premature beat
P-wave may look different
narrow QRS
what are the key findings of PAC on assessment?
primarily regular pulse
ooccasional early or irregular beat
otherwise asymptomatic
what is paroxysmal supraventricular tachycardia (PSVT)?
Re-entry at AV node
what are the ECG features of PSVT?
narrow QRS
P hidden / distorted
rate of 170-250
starts and stops abruptly or “bursts”
what are some mechanisms for long-term control of PSVT?
Calcium channel blockers
beta blockers
ablation therapy
if unstable: adenosine IV bolus
what is atrial flutter?
fleeting
re-entry
ischemic
usually resolves or converts to afiv
what are the key findings of atrial flutter on assessment?
flutter in chest
weak pulse low BP sluggish cap refill cyanosis pale syncope low uring output
what is an AFIB?
multiple uncontrolled re-entry circuits
what is a junctional escape beat / rhythm ?
sa node failed or is blocked at the AV node
what is heart block?
conduction block / delay in the AV node or bundle branches
what are the potential causes of heart block?
ischemia, infarction, increased PSNS tone, fibrosis, inflammation, surgery, drug toxicity, potassium imbalance, aortic valve disease, dilated myopathy
often associated with bradycardia and sometimes palpitations, can be temporary or permanent, may be drug induced from CCBs.
What is first degree heart block?
2nd degree?
3rd degree?
1st: PR interval delayed
2nd: PR interval delay + dropped QRS
3rd: dissociated P-wave and QRS complex.
what should we assess for when looking for heart block?
bradycardia, hypotension, if IHD may induce angina
signs and symptoms of low CO
how can we treat heart block ?
treatment depends on if it is temporary or permanent
treat underlying cause
- ischemia
- discontinue SNS / calcium blocking drug
- add or block PSNS (vagal)stimulation
pacemaker temporarily to keep pt safe while treating for underlying cause, then re-evaluate need for permanent pacemaker
what is the typical cause of first-degree AV block ?
digitalis (digoxin), iscnemia, increased potassium, beta blockers, ccbs
what is the typical cause of type 1 second degree AV block?
caused by digoxin, BBs
occurs w myocardial ischemia or infarction, but caused by increased PSNS activity
what is the typical cause of type 2 second degree AV block?
digitalis toxicity
often deteriorates to third degree Heart Block
what is third degree heart block?
COMPLETE heart block and AV dissociation
identify the 7 cardiac interventions and devices
pacemaker
cardiac resynchronization therapy (CRT)
ICD (implantable cardioverter defibrillator)
Cardioversion
Defibrillation
AED Automated External Defibrillator
CPR (cardiopulmonary resuscitation)
What is the refractory period?
time when the heart is unresponsive to further electrical stimulation.
prolonging the refractory period can terminate an arrhythmia
describe the vaughan williams classification of anti-dysrhythmic drugs.
CLASS I - Na Channel Blockers
CLASS II - Beta Blockers
CLASS III - K Channel Blockers
CLASS IV - CCBs
CLASS V - other
What are the 8 potential side effects of Anti-Arrhythmic drugs?
ALL anti-arrhythmics can cause arrhythmias
- hypersensitivity rxns
- nausea
- vomiting
- diarrhea
- dizziness
- blurred vision
- headache
Describe the function of Sodium channel blockers (Class I).
Membrane stabilizing drugs
suppress automaticity
further classified as Ia, Ib, and Ic
Describe the MOA of Procainamide as a class Ia sodium channel blocker
block sodium (FAST) channels
delay repolarization
increased Action Potential Depolarization
Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome
Describe the MOA of Lidocaine as a class Ib sodium channel blocker
Block sodium channels
accelerate repolarization and minimally decrease APD
Used for ventricular dysrhythmias only
provide 3 examples of Beta Blockers (class II)
- the LOLS
atenolol
esmolol
metoprolol
what is the MOA of beta blockers?
reduce / block SNS stimulation, thus reducing transmission of impulses in the heart’s conduction system
depress phase 4 depolarization
general myocardial depressants for both supraventricular and ventricular dysrhythmias
also used as anti-anginal and anti-hypertensive drugs
prevent or terminate tachyarrhythmias
provide an example of class III anti-arrhythmic drugs (potassium channel blockers)
Amiodarone
what is the MOA of Amiodarone?
inhibit K+ channels
prolong repolarization in phase 3
used for dysrhythmias that are difficult to treat, life threatening ventricular tachycardia, PSVT, ATRIAL FIBRILLATION OR FLUTTER
Long term use can lead to “amiodarone lung” - fibrosis
provide 2 examples of cardiac calcium channel blockers (class IV)
verapamil
diltiazem
what is the MOA of cardiac calcium channel blockers ?
inhibit slow-channel (calcium-dependent) pathways
decrease rate of spontaneous depolarization, which reduces the rate of pacemaker firing
slows conduction velocity within the AV node, lengthens the AV nodal EFP (effective refractory period)
used for PSVT,
describe digoxin as a class IV antidysrhythmic
used in AFIB, promoes rate control and increased contractility
last line in HF, has many side effects, impacts K level and is impacted by K level
describe adenosine as a class IV antidysrhythmic
inhibits AV node activity
used to terminate PSVTs that involve the AV node
used diagnostically to distinguish VT from PVST w aberrant conduction
describe magnesium sulfate (IV) as a class IV antidysrhythmic
bring serum magnesium to normal levels
membrane stabilizer
reduce likelihood of ventricular arrhythmias
