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cardio Flashcards

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1
Q

narrow-complex tachycardias originate

A

within/above the AV node

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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)

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3
Q

SVT: tx

A
  1. vagal: supine Valsalva
  2. adenosine 6-6-12 –> dilt + gtt
  3. synchronized cardioversion @100 J
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4
Q

tachyarrhythmia DDx: narrow, regular

A

sinus tach

aflutter

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5
Q

tachyarrhythmia DDx: narrow, irregular

A

afib w/wo variable block

multifocal atrial tachycardia

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6
Q

tachyarrhythmia DDx: wide, regular

A

VT

SVT w/aberrancy

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7
Q

tachyarrhythmia DDx: wide, irregular

A

torsades

SVT w/aberrancy

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8
Q

stable wide-complex tachycardia: tx

A

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

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9
Q

unstable wide-complex tachyarrhythmia: tx

A

synchronized cardioversion @200 J

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10
Q

unstable narrow-complex tachyarrhythmia: tx

A

synchronized cardioversion @50 J

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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

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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
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13
Q

How is BRASH different from pure AV nodal blocker intoxication?

A
  • presence of hyperK

- history (BRASH pts are usually medication-adherent)

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14
Q

3 most common causes of BRASH

A

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

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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
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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

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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
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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)

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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)
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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)

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21
Q

PQRST of OMI findings

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
A

STD maximal in V2-4

24
Q

Mobitz 1 vs 2

Study These Flashcards
A

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

25
3 things that determine RV function
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
RV spiral of death
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
6 steps of RV failure/crashing pulmonary HTN management
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
how to intubate in RV failure
* ** 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
complete heart block: what happens if the block is - at the AV node - infranodal
- 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
Why do you need to pace complete heart block?
escape rhythm isn't enough to maintain cardiac output
31
asymptomatic complete heart block: management
admit for cards evaluation
32
How does a right-to-left shunt work?
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
Eisenmenger's syndrome
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
How does asthma cause hypoxemia?
V/Q mismatch
35
How does PE cause hypoxemia?
V/Q mismatch
36
mitral valve prolapse: most common sx (+ tx)
palpitations, dyspnea, nonexertional CP, fatigue | - beta-blockers
37
mitral valve prolapse: murmur and how to affect it
mid-systolic click > mid-/late systolic murmur that increases w/lower preload (inverse relationship)
38
Takotsubo cardiomyopathy: prognosis
most people recover EF completely within a month
39
when to avoid nitro in cardiac pts
HOCM, preload-dependent states
40
During what time period can women develop peripartum cardiomyopathy?
last 3m of pregnancy until 5m postpartum
41
Kawasaki: strongest risk factor for development of coronary artery aneurysm
persistent fever despite treatment | - others: male, delayed diagnosis, < 1y or > 9y, failure to respond to initial IVIG
42
HOCM genetics
autosomal dominant
43
how to increase/decrease HOCM murmur
increase it by decreasing LV filling (i.e. standing, Valsalva) decrease it by increasing LV filling (squatting, T-burg)
44
Where are the needle Qs in a HOCM EKG?
lateral and inferior leads
45
HOCM tx
no vigorous activity beta-blockers calcium channel blockers NO INOTROPES OR NITRATES (WORSEN OBSTRUCTION)
46
Dressler's syndrome
pericarditis 2-10 weeks post-MI | tx: aspirin/NSAIDs, steroids, colchicine, stop anticoagulants 2/2 risk of hemorrhagic pericarditis
47
post-PCI rhythm that looks like VT
accelerated idioventricular rhythm: sign of reperfusion | looks like VT but is slower and a good sign!
48
cocaine chest pain tx
benzos nitrates phentolamine 1 mg
49
most common site of aortoenteric fistula formation
duodenum
50
capture and fusion beats: definitions, significance
``` capture = normal QRS when atria capture ventricles fusion = atria only depol partially, so QRS looks like a PVC ``` both found in VT (not SVT)

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