cardio Flashcards
narrow-complex tachycardias originate
within/above the AV node
wide-complex tachycardias originate
and one exception
below the AV node
(exception: SVT w/aberrancy, like a bundle branch block, rate-related conduction block, WPW, or a toxic-metabolic condition)
SVT: tx
- vagal: supine Valsalva
- adenosine 6-6-12 –> dilt + gtt
- synchronized cardioversion @100 J
tachyarrhythmia DDx: narrow, regular
sinus tach
aflutter
tachyarrhythmia DDx: narrow, irregular
afib w/wo variable block
multifocal atrial tachycardia
tachyarrhythmia DDx: wide, regular
VT
SVT w/aberrancy
tachyarrhythmia DDx: wide, irregular
torsades
SVT w/aberrancy
stable wide-complex tachycardia: tx
1st choice: amio 150 > gtt (or procainamide)
2nd choice: lido
don’t forget mag
unstable wide-complex tachyarrhythmia: tx
synchronized cardioversion @200 J
unstable narrow-complex tachyarrhythmia: tx
synchronized cardioversion @50 J
explain BRASH syndrome
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 is BRASH different from pure hyperK?
- 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 is BRASH different from pure AV nodal blocker intoxication?
- presence of hyperK
- history (BRASH pts are usually medication-adherent)
3 most common causes of BRASH
hypovolemia (GI loss, diuresis)
any cause of hypoperfusion
any cause of acute kidney injury
3 arms of BRASH tx
- 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
pressor choice in BRASH and rationale
low-dose epi (up to 10 mcg/min) to hit beta-1 receptors –> inotropy, and beta-2 receptors –> K shifting
symptomatic non-tox narrow-complex bradycardia: tx
- EKG, pads, and atropine 0.5 mg q3-5m, max 6 doses
- careful if there’s ongoing ischemia
- avoid if it’s wide-complex - epi 2-10 mcg/min
- TCP
- TVP
etomidate dosing for cardioversion
- 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)
progression of EKG findings during an untreated OMI
hyperacute T waves STE Q wave (1-12h) or STE w/TWI (2-5d) T wave recovery (weeks-months) permanent STE (LV aneurysm morphology)
progression of EKG findings when an OMI is reperfused
terminal TWI which eventually becomes symmetric
eventual return to baseline EKG (hours-days)
PQRST of OMI findings
P = pathologic Qs Q = QRS distortion (especially terminal) R = reciprocal changes S = shape of STs (straight = bad) T = T-waves (hyperacute)
OMI vs global supply-demand mismatch ischemia
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)
What EKG finding is posterior OMI until proven otherwise?
STD maximal in V2-4
Mobitz 1 vs 2
1: longer, longer, longer, drop
2: constant PRs, then drop (worse)
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)
RV spiral of death
pulmonary HTN = increased RV afterload
this causes:
- 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
- RV dilation > tricuspid regurg and RV failure
6 steps of RV failure/crashing pulmonary HTN management
- optimize fluid mgmt: use parasternal short, err on the side of restriction since these pts are typically overloaded
- maintain RV coronary perfusion: use pressors (norepi/vaso) rather than volume. The thin-walled RV doesn’t handle volume well.
- enhance RV inotropy: epi, dobutamine, or milrinone w/other pressors PRN to counteract hypotension
- 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 - support oxygenation/ventilation w/low TVs
- avoid NIPPV/intubation (increases RV afterload and drops RV preload) - treat the underlying cause
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
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
Why do you need to pace complete heart block?
escape rhythm isn’t enough to maintain cardiac output
asymptomatic complete heart block: management
admit for cards evaluation
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
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
How does asthma cause hypoxemia?
V/Q mismatch
How does PE cause hypoxemia?
V/Q mismatch
mitral valve prolapse: most common sx (+ tx)
palpitations, dyspnea, nonexertional CP, fatigue
- beta-blockers
mitral valve prolapse: murmur and how to affect it
mid-systolic click > mid-/late systolic murmur that increases w/lower preload (inverse relationship)
Takotsubo cardiomyopathy: prognosis
most people recover EF completely within a month
when to avoid nitro in cardiac pts
HOCM, preload-dependent states
During what time period can women develop peripartum cardiomyopathy?
last 3m of pregnancy until 5m postpartum
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
HOCM genetics
autosomal dominant
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)
Where are the needle Qs in a HOCM EKG?
lateral and inferior leads
HOCM tx
no vigorous activity
beta-blockers
calcium channel blockers
NO INOTROPES OR NITRATES (WORSEN OBSTRUCTION)
Dressler’s syndrome
pericarditis 2-10 weeks post-MI
tx: aspirin/NSAIDs, steroids, colchicine, stop anticoagulants 2/2 risk of hemorrhagic pericarditis
post-PCI rhythm that looks like VT
accelerated idioventricular rhythm: sign of reperfusion
looks like VT but is slower and a good sign!
cocaine chest pain tx
benzos
nitrates
phentolamine 1 mg
most common site of aortoenteric fistula formation
duodenum
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)
