conduction blocks, aortic diseases Flashcards
1
Q
first degree AVB
A
- prolonged PR
- 1:1 P to QRS
- not likely to degrade to second degree
- usu benign and asymptomatic
2
Q
treatment for first degree AVB
A
- if PR interval < 300 msec and narrow complex, no treatment
- if wide QRS refer to EP and possible pacemaker
- need to treat underlying causes
- avoid AV nodal blocking meds
3
Q
work up for second and third degree AVB
A
- check electrolytes
- check digoxin levels
- cycle cardiac biomarkers if suspect MI
- lyme titers
- echo
4
Q
Wenckebach
A
- aka mobitz type I
- PR interval gets longer and longer until dropped beat
- usually asymptomatic
- can happen in normal or sick hearts
- rarely progresses to complete heart block
5
Q
treatment of wenckebach
A
- treat underlying cause
- avoid AV nodal blocking meds
- no specific tx for asymptomatic pts
- monitor EKG for progression
- if syncope or other sx refer to EP
- if marked PR prolongation consider pacemaker
6
Q
Mobitz type II
A
- normal PR but random dropped beats
- indicates underlying disease of his- purkinje system
- sx range based on rate and frequency of dropped beats
- frequently progresses to complete heart block
7
Q
treatment for mobitz type II
A
- pacemaker in all pts
- treat underlying cause
- avoid AV nodal blocking meds
8
Q
third degree AVB
A
- complete AV dissociation
- disease of AV node or his- purkinje system
9
Q
clinical manifestations of third degree AVB
A
- chest pain if in setting of MI
- lightheadedness
- fatigue, weakness, exertional dyspnea
- bradycardia
- v tach or v fib
- asystole/ sudden death
10
Q
treatment for third degree AVB
A
- temporary pacer and refer to EP
- treat underlying cause
- avoid AV nodal blocking meds
- permanent pacemaker placement in all pts
11
Q
LBBB
A
- widened QRS > 0.12 sec
- broad S waves in V1-V3, AVR
- broad R waves in I, V5 V6
12
Q
treatment for LBBB
A
- if young and asymptomatic without CAD no treatment
- treat underlying cause
- manage and reduce risk in CAD
- if STEMI equivalent -> cath lab
13
Q
when is LBBB considered a STEMI equivalent
A
- new LBBB In setting of MI
- associated with increased short and long term mortality
- usually assoc with CAD
14
Q
aneurysm
A
- all three artery walls weaken -> abnormal bulge
15
Q
fusiform aneurysm
A
- entire circumference of segment of vessel
16
Q
saccular aneurysm
A
- portion of circumference -> out pouching of wall like a pocket
17
Q
pseudoaneurysm
A
- intimal and medial layers disruptued
- dilated segment lined by adventitia only
- doesnt involve all three layers
18
Q
etiology of aneurysm
A
- degenerative diseases
- atherosclerosis
- marfans
- ehlers- danlos
- family hx
- infections- tertiary syphilis
- vasculitis
- trauma
19
Q
thoracic aortic aneurysms
A
- most are in ascending aorta, next is descending
- assoc with atherosclerosis
- less common than AAA
- usually male with HTN in 50s or 60s
20
Q
diagnosis of TAA
A
- gold std= chest CT
- CXR
- echo
21
Q
sx of TAA
A
- often asymptomatic with normal PE
- if sx it is because aneurysm is very large
- chest, back, flank, or abd pain
- rarely HF sx
- hoarseness, wheezing, cough, hemoptysis, dysphagia
- rupture -> tachycardia and hypotension
22
Q
treatment of TAA
A
- BB, esp in Marfan
- HTN control, usually ACEI/ ARB
- operative repair / replacement when sx, ascending > 5.5 cm or descending > 6.5 cm
- may need endovasc repair
23
Q
AAA
A
- > 3 cm
- usu asymptomatic when > 5 cm
- rupture is catastrophic
- more common in men over 60
24
Q
at what point is AAA a concern for rupture
A
- > 5 cm
25
Q
where do most AAA occur
A
- 90% originate below renal arteries
26
Q
risk factors for AAA
A
- age > 60
- male
- cigarette smoking**
- HTN, hyperlipidemia
- caucasian, family hx
- other aneurysms
- atherosclerosis
27
Q
sx of AAA
A
- mostly asymptomatic
- abdominal, back, flank, or groin pain
- sudden cold or blue extremities
- any sx= rupture risk
- pulsatile abdominal mass
- eccchymosis if AAA ruptured
28
Q
screening for AAA
A
- abd US best
- men 65-74 with hx of cigarette smoking**
- first degree relative with hx of AAA
- pts with throacic or peripheral aneurysms
- pts with hypermobile syndromes like marfan’s or ehlers danlos
29
Q
treatment for AAA
A
- surveillance until > 5.5 cm
- open vs endovascular repair
- endovasc repair preferred- lower short term morbidity
- high mortality rate
30
Q
aortic dissection
A
- disruption of intima, blood pools between -> false lumen
- “intima dissects out from media”
- may lead to embolic phenomenon
- 90% occur in 1st 10 cm of aorta, most are 2.2 cm above aortic root
31
Q
risk factors for dissection
A
- HTN**
- atherosclerosis
- aortic aneurysm
- vasculitis
- marfan’s, ehlers- danlos
- bicuspid aortic valve, aortic coarctation
- previous cardiac surgery
- turner syndrome
- high intensity weight lifting
- crack, cocaine
32
Q
sx of dissection
A
- severe tearing back pain (intrascapular)
- pain may radiate to anterior chest or neck
- HTN
- wide pulse pressure
- unequal or diminished peripheral pulses
- chest pain + neuro sx
- acute aortic regurg
33
Q
diagnosis of dissection
A
- CXR and echo esp if pt is in acute distress
- CTA gold std
34
Q
findings on CXR for dissection
A
- widened mediastinum
- loss or aortic knob
- deviated trachea if dissection is large
35
Q
findings of CXR for AAA
A
- widened mediastinum
- tracheal deviation
36
Q
classification for dissection
A
- stanford type A- ascending aorta
- stanford type B- distal to left subclavian
- also the debakey classification
37
Q
treatment for dissection
A
- ascending- surgical emergency
- descending- medically managed
- operate if progression with end organ damage, continued hemorrhage, or tamponade
38
Q
surgical options for dissection
A
- endovascular repair or open surgical repair
- reoperation if extensive or recurrent dissection, aneurysm, or leakage at anastamoses or stent site
39
Q
medical therapy for dissection
A
- life long BB
- avoid strenuous activity
- keep BP < 120/80
40
Q
mortality rate for dissection
A
- 1% per hour for 72 hours if untreated
- over 90% at 3 months
