dysrhythmias Flashcards
1
Q
What are the sinus node rhythm disturbances?
A
- sinus arrhythmia
- sinus pause/sinus arrest
- sinus bradycardia
- sinus tachycardia
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
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
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
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
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
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
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
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
10
Q
Supraventricular arrhythmias?
A
- SVT
- AV node re-entrant tachycardia
- WPW
- atach
- afib
- aflutter
11
Q
Paroxysmal SVTs?
A
- AVNRT
- WPW
- atach
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
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
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
15
Q
Sxs of SVT?
A
- palpitations
- dizziness, light-headedness, or syncope (rare)
- SOB
- anxiety
- CP or tightness
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
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
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)
19
Q
sxs of WPW?
A
- palpitations
- tachycardia
- dizziness
- dyspnea
- anxiety
- syncope
- rarely: cardiac arrest
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
21
Q
Tx of WPW
A
- depends on frequency and assoc sxs
- radiofrequency ablation:
ablation of accesory pathways (very effective) - meds:
BBS
CCBs
flecainide
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
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
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
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
26
Q
Tx of PACs?
A
- asx: no special tx, just avoid precipitants
- sx: controlled with BBs
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
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
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
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
