Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

boards > cardio > Flashcards

cardio Flashcards

1
Q

narrow-complex tachycardias originate

A

within/above the AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

wide-complex tachycardias originate

and one exception

A

below the AV node
(exception: SVT w/aberrancy, like a bundle branch block, rate-related conduction block, WPW, or a toxic-metabolic condition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SVT: tx

A
  1. vagal: supine Valsalva
  2. adenosine 6-6-12 –> dilt + gtt
  3. synchronized cardioversion @100 J
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

tachyarrhythmia DDx: narrow, regular

A

sinus tach

aflutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

tachyarrhythmia DDx: narrow, irregular

A

afib w/wo variable block

multifocal atrial tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

tachyarrhythmia DDx: wide, regular

A

VT

SVT w/aberrancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

tachyarrhythmia DDx: wide, irregular

A

torsades

SVT w/aberrancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

stable wide-complex tachycardia: tx

A

1st choice: amio 150 > gtt (or procainamide)
2nd choice: lido
don’t forget mag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

unstable wide-complex tachyarrhythmia: tx

A

synchronized cardioversion @200 J

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

unstable narrow-complex tachyarrhythmia: tx

A

synchronized cardioversion @50 J

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

explain BRASH syndrome

A

bradycardia, renal failure, AV nodal blocker, shock, hyperK

  • bradycardia causes renal hypoperfusion/failure, which causes hyperK, which synergizes w/accumulated AV nodal blockers to worsen bradycardia and shock, which worsens renal failure

THE KEY = hyperK synergizing w/AV nodal blockers to cause bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is BRASH different from pure hyperK?

A
  • degree of hyperK: the hyperK in BRASH is usually milder; for hyperK alone to create bradycardia requires a more dramatic K
  • EKG w/only bradycardia (disproportionate): bradycardia w/o other EKG features of hyperK favors BRASH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is BRASH different from pure AV nodal blocker intoxication?

A
  • presence of hyperK

- history (BRASH pts are usually medication-adherent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 most common causes of BRASH

A

hypovolemia (GI loss, diuresis)
any cause of hypoperfusion
any cause of acute kidney injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 arms of BRASH tx

A
  • hyperK meds: calcium, insulin/dextrose, albuterol
  • IVF if hypovolemic: isotonic bicarb until acidosis resolves, then LR
  • kaliuresis: Lasix 80-160 +/- chlorothiazide 500-1000, Diamox 250-500, or fludrocortisone 0.2 PO (especially if pt is on ACEi) –> HD if failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pressor choice in BRASH and rationale

A

low-dose epi (up to 10 mcg/min) to hit beta-1 receptors –> inotropy, and beta-2 receptors –> K shifting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

symptomatic non-tox narrow-complex bradycardia: tx

A
  1. EKG, pads, and atropine 0.5 mg q3-5m, max 6 doses
    - careful if there’s ongoing ischemia
    - avoid if it’s wide-complex
  2. epi 2-10 mcg/min
  3. TCP
  4. TVP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

etomidate dosing for cardioversion

A
  1. 1 mg/kg –> second dose 0.05 mg/kg just before shock

i. e. 8 mg –> 4 mg (80 kg), or 10 mg –> 5 mg (100 kg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

progression of EKG findings during an untreated OMI

A 
hyperacute T waves
STE
Q wave (1-12h) or STE w/TWI (2-5d)
T wave recovery (weeks-months)
permanent STE (LV aneurysm morphology)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

progression of EKG findings when an OMI is reperfused

A

terminal TWI which eventually becomes symmetric

eventual return to baseline EKG (hours-days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PQRST of OMI findings

A 
P = pathologic Qs
Q = QRS distortion (especially terminal)
R = reciprocal changes
S = shape of STs (straight = bad)
T = T-waves (hyperacute)
22
Q

OMI vs global supply-demand mismatch ischemia

A 
OMI = localizes to an anatomic lesion
demand = does not localize - instead, shows diffuse STD (usually maximal in V4-6 and II w/STE in aVR)
23
Q

What EKG finding is posterior OMI until proven otherwise?

A

STD maximal in V2-4

24
Q

Mobitz 1 vs 2

A

1: longer, longer, longer, drop
2: constant PRs, then drop (worse)

25
Q

3 things that determine RV function

A

preload (more dependent on volume loading than pressure to accomplish work)

pump (contractility)

afterload (working against less than LV, since PVR is 1/10 of SVR)

26
Q

RV spiral of death

A

pulmonary HTN = increased RV afterload

this causes:

  1. prolonged isovolemic contraction > increased myocardial wall stress, wall hypertrophy, and septal shift > LV failure from impaired filling/contractility, RV ischemia, and decreased R coronary perfusion > RV failure
  2. RV dilation > tricuspid regurg and RV failure
27
Q

6 steps of RV failure/crashing pulmonary HTN management

A
  1. optimize fluid mgmt: use parasternal short, err on the side of restriction since these pts are typically overloaded
  2. maintain RV coronary perfusion: use pressors (norepi/vaso) rather than volume. The thin-walled RV doesn’t handle volume well.
  3. enhance RV inotropy: epi, dobutamine, or milrinone w/other pressors PRN to counteract hypotension
  4. reduce RV afterload: inhaled iNO or epoprostenol to dilate pulm vasculature only in ventilated areas > improves VQ mismatch and oxygenation
    - avoid systemic pulm vasodilators (IV, PO) unless pt is already on them; they cause systemic hypotension and worsen oxygenation
  5. support oxygenation/ventilation w/low TVs
    - avoid NIPPV/intubation (increases RV afterload and drops RV preload)
  6. treat the underlying cause
28
Q

how to intubate in RV failure

A
  • ** AVOID THIS ***
  • ** INTUBATION CAN PRECIPITATE HEMODYNAMIC COLLAPSE ***

must avoid any changes in hemodynamics = Fentanyl and ketamine awake w/video
- consider fiberoptic

in all cases:

  • good access
  • arterial line
  • push-dose epi and norepi/epi gtt already hanging
  • optimize volume status

if emergent:

  • RSI w/etomidate
  • anticipate hemodynamic collapse
  • premedicate w/10-20 mcg push-dose and 1-2U vaso just prior to induction even if not hypotensive
29
Q

complete heart block: what happens if the block is

  • at the AV node
  • infranodal
A
  • at the AV node: narrow complex, junctional escape pacemaker at 40-60 bpm
  • can be a complication of an inferior OMI*
  • infranodal: wide complex, ventricular escape pacemaker at 40 bpm or less
30
Q

Why do you need to pace complete heart block?

A

escape rhythm isn’t enough to maintain cardiac output

31
Q

asymptomatic complete heart block: management

A

admit for cards evaluation

32
Q

How does a right-to-left shunt work?

A

deoxygenated R-sided blood enters the systemic circulation because

  • anatomic shunt: congenital heart disease
  • physiologic shunt: nonventilated lung segments (i.e. ARDS, consolidation)

supplemental O2 won’t help

33
Q

Eisenmenger’s syndrome

A

an uncorrected left-to-right shunt goes on for so long that it increases pulmonary blood flow to the point of pHTN > compensatory RV hypertrophy > RV pressures surpass LV pressures, changing the direction of the shunt

34
Q

How does asthma cause hypoxemia?

A

V/Q mismatch

35
Q

How does PE cause hypoxemia?

A

V/Q mismatch

36
Q

mitral valve prolapse: most common sx (+ tx)

A

palpitations, dyspnea, nonexertional CP, fatigue

- beta-blockers

37
Q

mitral valve prolapse: murmur and how to affect it

A

mid-systolic click > mid-/late systolic murmur that increases w/lower preload (inverse relationship)

38
Q

Takotsubo cardiomyopathy: prognosis

A

most people recover EF completely within a month

39
Q

when to avoid nitro in cardiac pts

A

HOCM, preload-dependent states

40
Q

During what time period can women develop peripartum cardiomyopathy?

A

last 3m of pregnancy until 5m postpartum

41
Q

Kawasaki: strongest risk factor for development of coronary artery aneurysm

A

persistent fever despite treatment

- others: male, delayed diagnosis, < 1y or > 9y, failure to respond to initial IVIG

42
Q

HOCM genetics

A

autosomal dominant

43
Q

how to increase/decrease HOCM murmur

A

increase it by decreasing LV filling (i.e. standing, Valsalva)
decrease it by increasing LV filling (squatting, T-burg)

44
Q

Where are the needle Qs in a HOCM EKG?

A

lateral and inferior leads

45
Q

HOCM tx

A

no vigorous activity
beta-blockers
calcium channel blockers

NO INOTROPES OR NITRATES (WORSEN OBSTRUCTION)

46
Q

Dressler’s syndrome

A

pericarditis 2-10 weeks post-MI

tx: aspirin/NSAIDs, steroids, colchicine, stop anticoagulants 2/2 risk of hemorrhagic pericarditis

47
Q

post-PCI rhythm that looks like VT

A

accelerated idioventricular rhythm: sign of reperfusion

looks like VT but is slower and a good sign!

48
Q

cocaine chest pain tx

A

benzos
nitrates
phentolamine 1 mg

49
Q

most common site of aortoenteric fistula formation

A

duodenum

50
Q

capture and fusion beats: definitions, significance

A 
capture = normal QRS when atria capture ventricles
fusion = atria only depol partially, so QRS looks like a PVC

both found in VT (not SVT)

boards (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions