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Cardio II Exam 3 > AV Block, A Fib, PVC's > Flashcards

AV Block, A Fib, PVC's Flashcards

1
Q

what are the major causes of AV block ?

A
  1. increased vagal tone (sweaty, bradycardic, syncope)
    - stimuli could be sight of blood, could be drugs
  2. fibrosis and sclerosis of conduction system
    (SA –> internodal tracts –> AV node)
  3. IHD
    (tied in with fibrosis and sclerosis)
  4. cardiomyopathy and myocarditis
  5. congenital heart disease
  6. familial AV block
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2
Q

“AV node”

A

= protector of ventricles, protects A fib from going to Vfib, unless have WPW and bundle of kent

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3
Q

other causes of AV block?

A

hyperkalemia, infiltrative malignancies, neonatal Lupus, severe hypo or hyperthyroidism, trauma, degenerative neuromoscular diseases (lead to scarring and fibrosis of conduction system)
ex. myotonic dystrophy

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4
Q

which CCB’s cause AV block?

A

verapamil, diltiazem (non-DHPs) - decrease left ventricular fn: negative inotropes and negative chronotrops, will cause more AV/heart block

** don’t use with beta blockers:

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5
Q

drugs that cause AV block?

A

Digitalis, calcium channel blockers, beta blockers, amiodarone (long half-life), adenosine (used for blocking fast AV node re-entral mechanisms)

  • all of these have profound AV block

don’t use CCB’s and Beta blockers together

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6
Q

Iatrogenic (consequence of medical tx) AV block?

A
  1. Drugs: Digitalis, calcium channel blockers, beta blockers, amiodarone, adenosine
  2. Cardiac Surgery
  3. Catheter ablation of arrhythmias
  4. Transcatheter VSD closure (interrupts conduction system below the AV node)
  5. Alcohol Septal ablation for
    HOCM (hyperobstructive coronary myopathy - put catheter into septal branch, occlude it with balloon and inject alcohol, kills myocardium and this part of myocardium that is causing obstruction goes away… causes a mild MI due to the chemical irritant and heart block almost always happens transiently)
  6. TAVr (Transcatheter AV replacement)
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7
Q

normal PR interval?

A

0.2 seconds

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8
Q

first degree AV block?

A

PR interval of longer than 0.2 seconds at normal heart rates

  • when PR interval gets long, the atria is contributing its blood way before ventricle contracts and filling isn’t as efficienct –> results in decreased CO
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9
Q

rheumatic heart disease

A

mitral valve stenosis –> pulmonary HTN –> right heart failure

  • fixing the mitral valve, 90% of the time will result in alleviation of pulmonary HTN
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10
Q

AV block defintion

A

AV Block is defined as a delay or interruption in the transmission of an impulse from the atria to the ventricles due to an anatomic or functional impairment in the conduction system.

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11
Q

fibrosis and sclerosis and AV block

A

Fibrosis and sclerosis of the conduction system accounts for about 50% of cases of AV block and may be induced by several different conditions that often cannot be distinguished clinically. These are frequently progressive to complete heart block.

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12
Q

IHD and AV block?

A

IHD (Ischemic Heart Disease) accounts for 40% of cases. Conduction disturbances range from first degree AVB to complete with either chronic IHD or an Acute MI.

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13
Q

familial AV block

A

transmitted with autosomal dominant trait

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14
Q

drugs that cause AV block?

A

digitalis, calcium channel antagonists (verapamil and diltiazem), amiodarone, adenosine, and beta blockers can impair AV conduction, occasionally resulting in AV block.

Most are at least partially reversible following drug withdrawal

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15
Q

procedures that can cause AV block?

A

valve replacement, catheter ablations, closure of VSD’s, alcohol septal ablations and TAVr

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16
Q

Second degree AVB, Mobitz Type 1

A

= Wenchebach
progressive PR interval prolongation precedes a nonconducted P wave

count the P waves to the QRS complexes: ex. 5 to 4, Wenchebach

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17
Q

Second degree AVB, Mobitz Type 2

A

PR interval remains unchanged prior to a P wave that suddenly fails to conduct to the ventricles

if QRS is preceded by 4 p waves, then it would be 4:1, if HR is 80, then you would have a beat of 20

  • this is FIXED!
  • in a 2:1 sinus node senses this, it might bring the sinus beat up to 180 and would results in 90 bpm in a young person, however this effect would not be possible in an older person
  • Mobitz type II - will almost always need pacemakers
18
Q

third degree AVB

A

complete heart block, no atrial impulses get through

  • The block can exist in the AV node or in the infranodal specialized conduction system.
  • will need pacemakers
19
Q

concave vs. convex up ST segment elevation?

A

acute injury: see up sloping convex of elevated QRS complex

concave up sloping of ST segment is not normally MI

20
Q

QRS wide?

A

likely pacemaker is indicated

21
Q

QRS narrow?

A

pacemaker is not indicated

22
Q

Atrial fibrillation

A
  • most common cardiac arrhythmia in adults
  • the RR interval follows no repetitive pattern
  • no distinct P waves, undulating baseline
  • atrial rate is b/w 300-600 bpm
  • AF reduces CO (thus increased heart rate necessary in exercise) by decreasing filling from increased rate encroaching on diastolic filling time and loss of atrial contribution to ventricular filling
  • increases with age and is more common in men
23
Q

risk factors of AF?

A
  1. Hypertensive Heart Disease
  2. CHD
  3. RF in underveloped countries**
24
Q

paroxysmal-AF

A

terminates spontaneously or with intervention within 7 days of onset. Episodes may recurr with variable frequency.

25
Q

persistent-AF

A
  • fails to self-terminate within 7 days. Episodes often require pharmacologic or electrical cardioversion to restore NSR (Normal Sinus Rhythm). AF generally progresses.
  • usually gets worse as pt. gets older
26
Q

long standing persistant AF

A

AF that has lasted for more than 12 months.

27
Q

permanent AF

A

patients with persistant AF where a joint decision has been made by the patient and clinician to no longer pursue a rhythm control strategy.

28
Q

Low risk AF

A
  • Used to be called “Lone” AF.
  • 15-30% of AF
  • Younger male patients
  • Frequently familial, low risk of thrombo-embolus (CHADS2 score of 0).
29
Q

recurrent AF

A
  • 90% of AF patients have asymptomatic recurrent episodes lasting up to 48 hours
  • hard to know if they have ever had Afib before
30
Q

subclinical AF

A

AF detected in asymptomatic patients without a prior diagnosis. Many of these patients have paroxysmal AF.

31
Q

evaluation of pt. with AF?

A
  1. H&P
  2. History of palps, syncope, dyspnea, fatigue. Precipitating causes include exercise, emotion, alcohol- Holiday Heart. (alcohol related dysrhthmias, due to binge drinking)
  3. PE-mitral valve disease, especially Mitral stenosis, CHF findings, etc.
32
Q

evaluation of pt. with a fib?

A

EKG-rhythm, rate, other abnormal findings, LVH, ST changes, QRS width, QT interval, PR interval.

Echocardiogram-chamber sizes and function, valvular function, pulmonary artery pressures (Pulmonary Hypertension).

  • will show if pt. has mitral valve disease and if you have valvular or nonvalvular A fib
  • pulmonary HTN is very common at our altitude
33
Q

tx of a fib?

A

“tale of 2 cities” - both are equal except in people with CHF

  1. Rate Control- patient is appropriately anti-coagulated and the rate is controlled by AV blockers. (determine risk of stroke based on CHAD score or CHAD-VAS score) - use drugs to block AV node (Beta-blockers best! CCBs are never as good, verapamil and diltiazem do slow down the rate, but the can damage pt. with CHF)
  2. Rhythm Control- effort is made to anti-coagulate and restore NSR by meds or electrical cardioversion. A TEE may be used to rule out LA thrombus prior to cardioversion. (every effort is made in order to restore normal sinus rhythm to the patient)

TEE = trans-esophageal echo, used to rule out if there is a clot

34
Q

CHADS

A 
CHF = 1 pt
HTN = 1 pt
Age of 76+ = 1 pt
DM = 1 pt
Stroke/TIA = 2 points

*** score of 2+, give anticoagulant

35
Q

CHADS-VASc

A 
CHF = 1 pt
HTN = 1 pt
Age of 75+ = 2 pts (65-74 get 1 pt)
DM = 1 pt
Stroke/TIA = 2 points

female sex = 1 point

if have all 9 points, risk of stroke is 15% per year

*** if have 3 points = 3 percent per year, which is higher than risk of anticoagulant, score of three or above, give anticoagulant

36
Q

PVC’s

A

= premature ventricular beat - one of must common presenting complaints to cardiologists office

  • ALMOST ALWAYS NO SIGNIFICANCE!!!!
  • often overemphasized by pt. and occasionally by PCP
  • causes heart to pause, resulting in stronger/forecful, more volume ejected in following beat
  • patient will feel the pause or the beat after the pause felt in their upper carotids (due to volume or pressure receptors in aortas) –> make the patient want to cough
  • if patients are having every other beat = bigeminy
  • presents with palpitations
  • ** syncope is an alarm that IS serious: could be having sustained VTach
37
Q

when do PVC’s become a problem?

A

***** syncope is an alarm that IS serious: could be having sustained VTach

other than this it is almost always of no significance

38
Q

Look at rhtyhm strips!

A

do it now!

39
Q

what is a bad prognostic sign of PVC?

A

Presence of PVC’s with ACS (Acute Coronary Syndromes) is a bad prognostic sign, but the rules for PVCs in healthy individuals are totally distinct from these patients, and are almost always benign.

  • often pt. gets PVC’s due to stress, drugs, etc.
40
Q

Why do PVC’s occur?

A

Occur in patients without structural heart disease, and with various levels of severity of heart disease.

Frequency and complexity have no bearing on prognosis, only in ACS and post MI.

The severity of LV function determines prognosis, not the frequency or complexity of the PVCs.

Cardio II Exam 3 (15 decks)

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