Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/39

Click to flip

39 Cards in this Set

  • Front
  • Back
What are pacemakers?
Ectopic electrical signal sent to heart; used for certain bradyarrhythmias
Indications of using a pacemaker -
• Indications: Mobitz II AV block, 3° AV block, symptomatic bradycardias
• Not indicated: asymptomatic bradycardias that are unlikely to cause danger
Etiology of some arrhythmias -
Structural disease: may cause abnormalities in impulse conduction
• Scars: resulting from ischemia, cardiac injury. Scars are composed of fibrotic tissue, which does not conduct impulses, and viable tissue, which does. This mish-mash of variably conducting tissue may result in an anterograde block or a re-entry loop.
• Congenital abnormal connections: conducting tissue where there should not be any, either within the AV node (microcircuit re-entry), or outside the valves on the wall of the myocardium (macrocircuit re-entry)
Long QT syndrome -
This heritable condition gives a long QT due to prolonged ventricular repolarization, and anything that prolongs QT can lead to torsades de point → sudden cardiac death.

# of diff forms of QT - some auto. dom, some auto recc

Not everybody who has gene has EKG finding
Not everyone with EKG findings have problem
Brugada sydnrome -
persistent ST elevations in V1-V3
RBBB ECG pattern.
Causes sudden cardiac death
Young Asian males are more affected.
Hypertrophic cardiomyopathy -
hypertrophy results in stretching of conduction fibers & disorganization, which can lead to lethal arrhythmias
RVOT -
LBBB seen with wide complex QRS tachycardia (ie ventricular tachycardia).

Generally asymptomatic and not dangerous, but must be differentiated from other dangerous ventricular tachycardia’s -> can appear in nL heart; not lethal

Tx with meds and ablation
RV dysplasia -
RV cardiomyopathy
Hallmark on EKG - Inverted T wave lead 1-3

Look for fatty infiltration of RV
Dx: MRI, not biopsy
What is sinus bradycardia?
sinus means atria beat before ventricles (P wave precedes QRS wave)
What is sick sinus syndrome?
SA node dysfunction resulting in sinus brady, pause, arrest
What is tachybrady syndrome?
subset of SSS, with alternating sinus brady & tachy
What is vasovagal reaction?
pain, anxiety, stress → sympathetic/parasympathetic response
o Increase in parasympathetic vagus nerve → bradycardia
o Decrease in sympathetic tone → vasodilation leading to hypotension
Reasons for iatrogenic sinus bradycardia?
o Drugs: β-blockers, CCBs, parasympathomimetics, digoxin, antiarrhythmics
o Procedures: damage to conducting system can occur during cardiac catheterization, EP studies, other surgery → scar tissue does not conduct impulses
Reasons for ischemic mediated bradycardia?
infarct of coronary artery may cause ischemia to SA and AV nodes
o RCA: usually supplies both SA and AV nodes
o LAD: may supply SA node, depending on anatomy
1st degree AV block -
delay across the AV node reflected as PR interval > 0.2s, but every atrial impulse still results in a ventricular beat (1:1 conduction)
2nd degree AV block (Wenckeback's) type 1 -
PR interval progressively prolongs and then QRS wave drops out
o Block is located in the AV node
Not usually indicated for pacemaker
2nd degree Morbitz type II AV block -
QRS wave drops out without a graduation of PR interval
o Block is located in His Bundle
Usually indicated for pacemaker
3rd degree AV block -
no association between atrial impulses and ventricular beats
o Block is located in either AV node or His Bundle
• Premature ventricular contraction (PVC
ectopic beat arising from ventricle, seen as a wide complex QRS not preceded by a P wave
Etiology, presentation and tx of PVC -
o Etiology: hypoxia, electrolyte abnormality, hyperthyroidism, stimulants
o Presentation: usually asymptomatic, may feel palpitations
o Treatment: β-blockers if symptomatic, ICD is repetitive PVCs (risk of VFib)
Ventricular tachycardia -
tachycardia originating below bundle of His, defined as a rapid firing of 3+ PVCs in a row at a rate above 100 bpm
Etiology. presentation, treatment of VT -
o Etiology: CAD, MI, cardiomyopathies, congenital heart defect, congenital QT
o Presentation: asymptomatic if nonsustained. Sustained VT (>30 seconds) usually symptomatic with palpitations, hypotension, angina, syncope; may lead to VFib
o Treatment: antiarrhythmics and/or cardioversion & ICD placement
What is Torsades de point?
Etiology
Presentation
Treatment
a type of ventricular tachycardia characterized by polymorphous QRS complexes in a shifting sinusoidal pattern, preceded by a prolonged QT

o Etiology: QT syndrome, class III antiarrhythmics, TCAs, hypocalcemia/kalemia/magnesemis, structural heart disease, ischemia
o Presentation: palpitations, dizziness, syncope, sudden death
o Treatment: Mg+ provides cardiac stabilization, address underlying disorder
What is ventricular fibrillation?
multiple foci of ventricles fire randomly leading to quivering ventricles and no CO, seen as erratic QRS complexes
Etiology/Presentation/Tx of Vfib -
o Etiology: ischemic heart disease, torsades, combination of Afib + WPW
o Presentation: syncope, no blood pressure, pulselessness, death
o Treatment: immediate defibrillation and CPR → advanced cardiac life support
What are SVTs and 3 main causes of it -
SVTs: tachycardias that originate above the ventricles, occurring as a result of the following -

1. Increased/abnormal automaticity
2. Triggered activity (EAD/DAD)
3. Re-entry
Explain increased/abnL automaticity -
change in activity within the atria due to…
a. Increased sympathetic stimulation of SA node
b. Cells outside SA node start to spontaneously depolarize
c. Change in resting membrane potential (ie from ischemia, electrolyte abnormalities) making it easier to depolarize
Explain triggered activity
abnormal depolarization triggered by a previous beat
a. Early after depolarization: depolarization before repolarization is complete
i. Increase in time of repolarization (extended opening of Ca channels during phase 2, or opening of Na channels during phase 3)
ii. Due to ischemia, hypokalemia, catecholamine excess, mechanical injury
b. Delayed after depolarization: depolarization after repolarization, but before a normal AP normally occurs (phase 4)
i. Excess Ca within the SR of cell resulting in spontaneous depolarization
ii. Due to digitalis toxicity, hypokalemia, hypercalcemia, catecholamines
Explain re-entry -
accessory pathway exists, where impulses can travel retrograde and back around to original pathway; requires unidirectional block with slow conduction in other pathway to allow enough recovery time for reentry
a. Micro-reentrant: occur within the AV node = AV Nodal reentrant tachycardia
b. Macro-reentrant: outside the AV node = AV reentrant tachycardia
What is Afib?
most common arrhythmia
• Description: multiple foci in atria fire continuously and in a chaotic pattern, resulting in a quivering atria & irregular rapid ventricle. Impulses commonly originate around the pulmonary veins. Classified as paroxysmal or continuous/refractory.
o ECG: no P waves, irregularly irregular QRS waves
Etiology of Afib -
HTN, valve disease, CAD, thyrotoxicosis, EtOH (holiday heart syndrome), pericardial disease, COPD, pheochromocytoma, sick sinus syndrome
• Presentation: range from asymptomatic to dyspnea, fatigue, palpitations; irregularly irregular rhythm on physical exam
o Complications: stroke, other embolic disease, angina, hypotension, syncope
Treatment of Afib -
rate control & anticoagulation >>> rhythm control & symptoms
o Rate: β-blockers or calcium channel blockers
o Anticoagulation: aspirin for low risk, warfarin for high risk (CHADS score)
o Rhythm: consider anti-arrhythmics, usually amiodarone
o Symptoms usually controlled with rate control, but some still feel symptomatic
• Cardioversion: shock the heart back into sinus rhythm (Note: unless the patient has been on therapeutic warfarin therapy, must do Echo to rule out ventricular thrombus)
• Ablation: ablate around the pulmonary veins; usually last ditch effort
Atrial flutter -
• Description: single automaticity focus in atria fires at 250-350 bpm, with atrial impulses being transmitted to the ventricles in a predictable pattern (2:1 or 3:1 conduction)
o ECG: sawtooth pattern (atrial contractions)
Etiology/presentation/treatment of Afib -
• Etiology: CAD, CHF, valvular disease, COPD
• Presentation: fatigue, palpitations, embolic disease (similar to A fib)
• Treatment: similar to A fib, except ablation is more effective
Wolff-Parkinson-White disease -
• Description: accessory pathway from atria to ventricles called the Bundle of Kent, located in the atrioventricular valvular rings. Pathway does not share the rate controlling properties of the AV node, allowing early depolarization of part of the ventricle
o ECG: short PR interval, delta wave, widened QRS
Etiology, presentation, treatment of WPW -
• Etiology: congenital
• Presentation: asymptomatic to syncope, palpitations
o Atrial premature beat may lead to orthodromic reciprocating tachycardia (reentry loop through accessory pathway, without a delta wave) or antidromic AVRT
o Atrial fibrillation with WPW can lead to ventricular fibrillation & sudden death
• Treatment: risk stratification – look for risk of atrial tachyarrhythmias on top of WPW, which predisposes to sudden death
o Ablation: very successful
o Avoid drugs that slow AV conduction because that may increase conduction through the accessory pathway
Atrioventricular & AV Nodal re-entrant tachycardia -
• Description: (1) Sinus beat conducted down both the fast & slow pathways. (2) Premature atrial contraction shoots out of the atria, but the fast pathway is still refractory, giving a unidirectional block. (3) Conduction through the slow pathway results in retrograde conduction via the fast pathway.
o AVRT: pathways located around the valves
o AVNRT: pathways within the AV node
o ECG: note upside down P wave (above); may have narrow or wide QRS depending on which pathways is depolarizing the ventricles
Atrioventricular & AV Nodal re-entrant tachycardia etiology -
• Etiology: ischemic heart disease, digoxin toxicity, caffeine/alcohol may exacerbate
• Presentation: may feel palpitations, generally not dangerous
Atrioventricular & AV Nodal re-entrant tachycardia treatment -
(1) Maneuvers (Valsalva, carotid massage, breath holding, head immersion in cold water) to stimulate vagus delay of AV conduction. (2) Adenosine decreases AV nodal activity. (3) Electric cardioversion.
• Ablation if episodes are recurrent and symptomatic