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dysrhythmias Flashcards

1
Q

What are the sinus node rhythm disturbances?

A
  • sinus arrhythmia
  • sinus pause/sinus arrest
  • sinus bradycardia
  • sinus tachycardia
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2
Q

What age group is sinus arrhythmia common in?

A
  • younger pts

- not common in older pts due to age related decrease in parasympathetic tone

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3
Q

What does sinus arrhythmia look like on an EKG?

A
  • rate: variable
  • P: normal
  • PR: normal
  • QRS: normal
  • rhythm: sometimes appears irregular, but originating from the sinus node
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4
Q

What does sinus arrhythmia sync with? Tx?

A
  • synchronizes with respiratory cycle: inspiratory reflex inhibition of vagal tone
  • cyclic variation in HR
  • tx: benign, requires no tx
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5
Q

When does sinus pause/arrest occur?

EKG presentation?

A
  • healthy hearts
  • vagal tone
  • myocarditis
  • MI
  • digitalis toxicity
  • pause lasts 2 seconds to 2 minutes
  • normal and fixed PR intervals and R-R intervals and lack of P wave
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6
Q

Tx for sinus pause/arrest?

A

depends on underlying condition

  • pacemaker
  • atropine for hemodynamically unstable ( parasympathetic - increases HR), tx for bradycardia. Short term tx
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7
Q

What is sinus bradycardia?
who is it common in?
What is it caused by?

A
  • HR less than 60 bpm
  • common in young adults (athletes)
  • caused by: BBs or digoxin
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8
Q

Tx of sinus bradycardia?

A
  • only tx if sxs of HTN or dizziness
  • short term: atropine, tempory pacer
  • asx: monitor and educate
  • long term: pacemaker if sx
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9
Q

What is sinus tachycardia?

  • causes
  • tx?
A
  • HR more than 100 bpm
  • causes: fever, pain, exercise, anemia, hypotension, increased catecholamines, thyrotoxicosis, anxiety
    tx: underlying cause,
    CCB: diliazem, verapamil
    BBs: for sx tachycardia
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10
Q

Supraventricular arrhythmias?

A
  • SVT
  • AV node re-entrant tachycardia
  • WPW
  • atach
  • afib
  • aflutter
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11
Q

Paroxysmal SVTs?

A
  • AVNRT
  • WPW
  • atach
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12
Q

SVTS origin?

A
  • from above the HIs bundle
  • most commonly caused by reentrant circuit in AV node
  • likely to begin or end with premature atrial or ventricular contraction
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13
Q

SVT is most common in what age group? Could be caused by?

A
  • most common in young adults
  • most people are able to live without restrictions in activity, often occur in episodes with stretches of normal rhythm in b/t
  • may be a SE of meds or ilicit drugs:
    digitalis, asthma meds, or cold remedies, caffeine, ephedra, cocaine, meth
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14
Q

PSVT presentation on EKG?

A 
HR: 140-240
regular rate
P wave different from normal sinus rhythm P wave for that person
- p wave often buried in QRS
- QRS is narrow and of normal morphology
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15
Q

Sxs of SVT?

A
  • palpitations
  • dizziness, light-headedness, or syncope (rare)
  • SOB
  • anxiety
  • CP or tightness
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16
Q

Tx of SVT?

A
  • vagal maneuvers:
    hold breath for few seconds
    dip face in cold water
    cough
    tense stomach muscles as if bearing down to have BM
  • carotid massage, start at R side for 20 seconds then move to L (not at same time)
  • drug therapy: adenosine (adenocard) 6 mg IV: half life is less than 10 sec, given IV, fast push followed by NS flush, may be repeated with additional 6 mg and then 12 mg
  • adenosine works in more than 90% of cases
    blocks conduction at AV node
  • if adenosine is unsuccessful: consider cardioversion if pt is hemodynamically unstable (sedated)
    or IV BB (esmolol or propranolo) or CCB
    Therapy to prevent recurrence:
  • BBs (metroprolol)
    CCBs (diltiazem), digoxin
  • perm tx is SVT ablation
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17
Q

What is WPW?

A
  • form of SVT
  • accessory pathway that bypasses the AV node (bundle of kent)
  • along with normal conduction pathway, there are extra pathways - accessory pathways, they conduct impulses faster than normal, conduct impulses in both directions (HR typically greater than 200)
  • congenital defect, sxs can occur at any age
  • one of the most common causes of fast arrhythmia in infants and children
  • highest incidence b/t ages of 30-40
  • more common in men than women
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18
Q

What is the greatest concern for people with WPW?

A
  • possibility of having afib with a fast ventricular response that worsens to fib, a life threatening arrhythmia (can worsen to V fib)
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19
Q

sxs of WPW?

A
  • palpitations
  • tachycardia
  • dizziness
  • dyspnea
  • anxiety
  • syncope
  • rarely: cardiac arrest
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20
Q

EKG presentation of WPW?

A
  • seen only after rhythm conversion from PSVT to NSR
  • PR is shorter than 0.12 s
  • uptake of QRS is slurred, this is the delta wave (easier to see in precordial leads)
  • 12 lead is essential because delta wave may not show up on all leads
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21
Q

Tx of WPW

A
  • depends on frequency and assoc sxs
  • radiofrequency ablation:
    ablation of accesory pathways (very effective)
  • meds:
    BBS
    CCBs
    flecainide
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22
Q

How to terminate an acute episode?

A
  • vagal maneuvers
  • IV adenosine: 6-12 mg rapid IV push
  • or IV diltiazem or verapamil
  • have defb ready as meds may turn rhythm into fib
  • if hemodynamically unstable: cardioversion
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23
Q

What is PAT? Tx?

A
  • atrial rate of 150-250, may conduct to ventricles but AV node will try to block impulses
  • P wave: morphology usually varies from sinus, originates from an irritable atrial focus
  • may occur in normal as well as diseased heart
  • often transient and usually reqrs no tx
  • can usually be terminated with vagal maneuvers
  • if these fail: adenosine, or cardioversion, digoxin, BBs, CCbs - prevent recurrence
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24
Q

What are PACs?

A
  • d/c from non-sinus atrial pacemakers
  • P wave preceding may not look like P waves that originated from sinus node
  • very frequent PACs may be precursor to development of afib
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25
Q

who has increased likelihood of PACS?

A
  • can occur in all ages with or w/o disease
  • increased incidence with:
    mitral valve disease
    MI
    cardiomyopathy
    smoking
    alcohol
    caffeine
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26
Q

Tx of PACs?

A
  • asx: no special tx, just avoid precipitants

- sx: controlled with BBs

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27
Q

What is a wandering atrial pacemaker?

A
  • may occur in normal hearts as result of fluctuations in vagal tone
  • seen in pts with heart disease and COPD
  • rate: variable depending on site of pacemaker; usually 45-100 bpm
  • p wave: needs to have 3 distinctly diff P wave morphologies (may be seen after QRS interval)
  • usually no tx reqd
  • may also be precursor to multifocal atrial tach
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28
Q

What is multifocal atrial tach?

A
  • irregular cardiac rhythm caused by at least 3 diff sites of competing atrial activity
  • presence of 3 or more P wave morph on a given lead
  • heart rate greater than 100 bpm
  • it usually doesn’t cause hemodynamic instability
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29
Q

MAT is common in what pops and conditions?

A
  • underlying lung disease
  • COPD is the most common underlying cause
  • acute MI
  • sepsis
  • hypokalemia
  • theophylline toxicity
  • low magnesium
  • may be a precursor to afib
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30
Q

Tx of MAT?

A
  • directed at underlying medical problems

- may suppress rate witjh AV nodal blocking agents: CCBs and BBs

31
Q

What is Afib? EKG presentation?

A
  • most common encountered arrhythmia in practice
  • mult reentrant loops generate chaotic atrial depolarization (micro reentrant circuit)
  • AV node is bombarded with rates greater than 400 bpm from atrial foci
  • AV works hard to block impulses, ventricular rate is IRREGULAR IRREGULAR - bounding pulse
  • b/t 110-170 bpm
  • can be a slow rate as well: sign of sig underlying conduction disorder
  • No distinguishable P waves on EKG
32
Q

What conditions are Afib commonly found with?

A 
- underlying cardiac disease:
valvular disease
heart failure
ischemic heart disease
HTN
sleep apnea
33
Q

Afib can be precipitated by what conditions?

A
  • pericarditis
  • thyrotoxicosis
  • PE
  • pneumonia
  • acute alcohol ingestion
  • post op cardiac surgery
  • post op thoracotomy
  • sleep apnea
  • HTN
34
Q

Afib’s impact on the body? heart? EF?

A
  • EF may decrease 10% due to loss of atrial kick
  • HF if rapid rate isn’t controlled
  • emobolic stroke due to pooling of blood in atria
  • palpitations
  • SOB
  • poor exercise tolerance
  • worsening CHF or ischemic sxs
35
Q

Risk of stroke? Prevention of thromboembolic complications in Afib?

A
  • 5-6% risk of embolic stroke/year (cumulative)
  • stasis of blood in atria:
    warfarin (coumadin)
    2-3 INR
    pradexa, xalreto - new AC no INRs or dietary interactions
  • healthy pts: aspirin
36
Q

CHADS2 criteria? Who does it apply to?

A
  • CHF = 1 pt
  • HTN = 1
  • older than 75 = 1
  • DM = 1
  • stroke or TIA = 2 pts
  • if 2 pts or greater = anticoag unless CI
  • under 2 pts: 325 mg of aspirin
  • only applies to pts without valve disease
37
Q

How do we control rate in afib? What is a good rate to have?

A
  • ventricular rate b/t 60-110 had the same outcomes as pts who were converted to NSR
  • Diltiazem (cardizem)
  • BBs
  • digoxin (not first line)
38
Q

How do we restore sinus rhythm if necessary? antiarrhythmics?

A
  • class 1A antiarrythmics (only used with ACLS protocol):
    pronestyl (procainimide)
    quinidine (cardioquin)
  • class III antiarrhythmics:
    sotalol (betapace)
    ibutilide (corvet) IV only
    amiodarone (titrated up to 400 mg po qday)
    ** worry about long term toxicity issues, lungs, thyroid, liver and eyes need monitoring
  • class IC: used only in pts with structurally normal hearts (absence of CAD or cardiomyopathy) - propafenone (rythmol), and flecainide (tambocor)
  • cardioversion: less than 48-72 hrs of a-fib: safe to cardiovert (still might have to rule out thrombus)
  • if duration unknown: rate control, anticoag for 4-6 weeks than cardiovert, or anticoag for 6 weeks after successful cardioversion or indefinitely if pt was unaware of afib
  • ** TEE to see if atrial thrombus present to prior cardioversion
39
Q

What is next line of tx if cardioversion and medical therapy fail?

A
  • afib ablation

- av node ablation in extreme cases which would require permanent pacemaker placement

40
Q

Most feared complication of a fib? other complications?

A
  • stroke (especially in pts older tha 75) - clots occur more in LA
  • CHF
  • severe bradycardia
  • rate related MI (tachy or brady rhythm)
41
Q

Eval process of new onset afib pts?

A
  • eval for presence of valvular heart disease (echo)
  • eval for presence of ischemic heart disease (nuclear stress test)
  • rule out sleep apnea even in pts with normal BMI (sleep study)
  • thyroid function tests
42
Q

What is a flutter?

A
  • macro reentrant circuit
  • atrial rate: 250-350
  • ventricular rate: 150
  • AV node blocks at 2:1, 3:1, 4:1
  • can also have slow ventricular rate
  • regularly irregular
  • classic sawtooth pattern on EKG
  • almost always occurs in diseased hearts
  • it precipitates CHF
  • and may be a precursor to fib
  • may be precipitated by:
    thyrotoxicosis
    pericarditis
    alcohol ingenstion (causes afib)
  • rate is harder to control than afib
  • tx depends on hemodynamic compromise
    they should be at least getting 325 mg ASA daily
43
Q
  • Why is thrombolic event risk somewhat lower than afib?
A
  • because there is atrial contraction that is occuring in a flutter as opposed to afib
44
Q

Tx for aflutter?

A
  • ablation if failed cardioversion and medical therapy
  • class 1A antiarrythmics are used to convert to sinus rhythm: procainmide
  • ventricular rate controlled with: BBs, CCbs, and digoxin
45
Q

workup for aflutter?

A
  • thyroid studies
  • rule out structural and functional heart disease with echo
  • rule out ischemic heart disease with nuclear stress test
  • rule out sleep apnea
46
Q

AV node disturbances?

A
  • junctional escape rhythm: 40-60 bpm
  • accelerated junctional rhythm: 60-100 bpm
  • these 2 are common in pts with inferior MI, digoxin toxicity
  • junctional tachycardia
47
Q

EKG presentation of Junctional escape, accel junctional rhythm

A
  • narrow complex QRS
  • retrograde P wave:
    inverted P with very short PR interval, P wave right after QRS, or sometimes no P wave
  • specific tx is usually not required
48
Q

What is junctional tachycardia?

A
  • 150-250 bpm
  • occurs more commonly in women
  • may occur in absence of heart disease
  • usually initiated by a PAC
49
Q

tx for junctional tachycardia rhythms?

A
  • acute: vagal maneuvers, adenosine (DOC, terminates 95% of cases)
  • long term: BBs, CCBs, Class 1A, 1C, and III antiarrythmics for resistant cases
50
Q

AV blocks?

A
  • 1st degree
  • 2nd degree, mobitz type 1 (wenkebach)
  • 2nd degree, mobitz type 2
  • 3rd degree heart block (AV dissociation)
51
Q

When does 1st degree AV block occur?

A
  • occurs in both healthy and diseased hearts
  • can be due to:
    inferior MI
    digitalis toxicity
    hyperkalemia
    increased vagal tone
    acute rheumatic fever
    myocarditis
    EKG: PR greater than 0.20
52
Q

Tx of 1st degree AV block?

A
  • interventions include tx the underlying cause
  • usually don’t need any other tx
  • observe for progression to a more advanced AV block
53
Q

When does 2nd degree AV block-mobitz type 1 (wenckebach) occur? EKG presentation?

A
  • occurs in AV node above bundle of his
  • often transient and may be due to acute inferior MI or digitalis toxicity
  • tx usually not indicated as rhythm usually produces no sxs
  • EKG: rate may be variable, PR interval gets progressively longer until a QRS is dropped (or blocked)
  • observe for progression to more advanced AV block
54
Q

2nd degree AV block mobitz type 2?

A
  • usually occurs below bundle of his and may progress into higher degree AV block (more severe)
  • can occur after an acute anterior MI due to damage in the bifurcation or bundle branches
  • more serious than type 1
  • tx is usually artificial pacing, via external pacer or temporary pacer wire insertion
    tx: permanent pacemaker
55
Q

EKG findings of AV block - mobitz type II?

A
  • rate: variable
  • P wave: normal
  • QRS: usually widened because this is usually assoc with bundle branch block
  • PR: may be normal until dropped QRS
56
Q

What is a 3rd degree heart block (complete)?

A
  • block of atrial impulses occurs at AV junction, common bundle or bilateral bundle branches (no comm b/t atria and ventricles)
  • another pacemaker distal to block takes over in order to activate the ventricles or ventricular standstill occurs
  • atrial and ventricular activities are unrelated due to complete blocking of atrial impulses to the ventricles
57
Q

3r degree heart block findings on EKG?

A
  • atrial rate is usually normal
  • ventricular rate is usually less than 70 bpm
  • atrial rate is always faster than ventricular rate
  • P waves: normal with constant P-P intervals but not married to QRS complexes
  • QRS: may be normal or widened depending on where the escape pacemaker is located in conduction system
58
Q

Tx for 3rd degree heart block?

A
  • external pacing and atropine for acute, sx episodes

- perm pacing for chronic complete heart block

59
Q

Ventricular dysrhythmias?

A
  • PVCs
  • Vtach
  • V fib
  • asystole
  • idioventricular rhythm
  • PEA
60
Q

Causes of PVC’s

A
  • increasing circulating catecholamines
  • coronary ischemia
  • hypokalemia
  • low magnesium level
  • drug (digitalis) toxicities
  • hypoxemia
  • also occurs in normal hearts
61
Q

PVCs on EKG?

A
  • rate: variable
  • P wave: obscured by QRS with PVC
  • QRS: wide 0.12, morphology is bizarre: the impulse originates below the branching portion of the bundle of his
  • can have multifocal PVCs, R on T phenomenon (could be start of Torsades)
  • full compensatory pause is characteristic
    rhythm: looks irregular due to premature beat
  • PVCs may occur in singles, couplets, or triplets, or bigeminy, trigeminy, or quadrigeminy
62
Q

Tx for PVCs?

A 
- tx may be reqd if they are:
assoc with acute MI
occur as couplets, bigeminy, or trigeminy continuously
- are multifocal
- are frequent (more than 6 PVCs per minute) and are assoc with hemodynamic instability
- lidocaine: class 1B antiarrhymic
- procainamide (pronestyl): clas 1A
- amiodarone (cordorone): class 3 
- replace magnesium, K+ if appropriate
63
Q

V tach?

A
  • triggers of VT include ischemia and electrolyte abnormalities
  • hypokalemia: most impt arrhythmia trigger clinically followed by hypomagnesemia
  • hyperkalemia also may predispose to VT and VF, particularly in pts with structural heart disease
64
Q

Causes of Vtach?

A
  • MI: irritable ventricle
  • Congenital heart defects
  • dilated cardiomyopathy
  • hypertrophic cardiomyopathy
65
Q

What does V tach look like on EKG?

A
  • absent P waves
  • QRS greater than 0.12 because it arises from the ventricle
  • regular rate and characteristic morphology
  • classified as sustained: greater than 30 seconds or non sustained: less than 30 sec (NSVT)
  • sustained will usually cause hemodynamic instability
  • considered life threatening rhythm as it can degenerate to v fib
66
Q

Tx for V tach?

A
  • can have a pulse or be pulseless:
    pulse:
    cardioversion, antiarrhythmics to prevent recurrence: amiodarone
    pulseless: considered the same as VF: defibrillation, antiarrhythmics to prevent recurrence: amiodarone, refractory cases are tx with ablation
67
Q

Torsades de Pointes?

A
  • means twisting about the points, usually paroxysmal
  • hallmark of this is the upward and downward deflection of QRS complexes around the baseline
  • caused by:
    drugs which lengthen the QT interval
    electrolyte imbalances, particularly hypokalemia and hypomagnesemia
    MI
68
Q

Tx of Torsades?

A
  • synch cardioversion is indicated
  • IV magnesium
  • IV K to correct electrolyte imbalance
  • overdrive pacing
69
Q

V fib? Tx?

A
  • sudden cardiac death
  • dysrhymia results in absence of cardiac output
  • almost always occurs with serious heart disease, especially acute MI
  • course of tx:
    immed defibrillation and ACLS protocols
    ID and tx of underlying cause
    consider ICD
70
Q

Idioventricular rhythm? causes?

A
  • absent P wave, widened QRS, greater than 0.12 s
  • also called dying heart rhythm
  • pacemaker will most likeyl be needed to re-establish a normal heart rate

causes:

  • MI or infarction
  • pacemaker failure
  • metabolic imbalance
71
Q

Tx of idioventricular rhythm?

A
  • improve CO and est normal rhythm and rate
  • options are:
    atropine and pacing
  • caution: suppressing the ventricular rhythm is CI b/c that rhythm protects the heart from complete standstill
72
Q

What is asystole?

A
  • presence of acute MI an CAD: almost always fatal
  • complete cessation of any electrical or mechanical activity
  • interventions include: CPR, 100% O2, IV, intubation, transcutaneous pacing, epi IV push q 3-5 min, atropine
73
Q

What is pulseless electrical activity? (PEA)

A
  • there is electrical activity, but no mechanical response
  • what is seen on EKG is electrical activity appearing as normal sinus rhythm
  • there will be NO pulse
  • look for underlying causes - 6 Hs and 6 Ts:
    hypoxia, hypovolemia, hypoglycemia, H ion (acidosis), hypothermia, hypo/hyperkalemia
    toxins, tamponade, trauma, tension pneumothorax, thrombosis - cardiac, thrombosis - pulmonary
74
Q

Tx for PEA?

A
  • correct underlying cause
  • epi: 1:10,000
  • atropine
  • CPR

Cardiology (20 decks)

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