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95 Cards in this Set
- Front
- Back
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hyperkalemia EKG |
diffuse peaked Ts -> |
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hyperkalemia vs. MI?
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hyperkalemia: peaked Ts are diffuse
MI: peaked Ts only over infarct |
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hypokalemia EKG |
ST depression, flattened T, new U wave
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U wave best seen... |
in hypokalemia; |
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hypocalcemia EKG |
prolongs QT interval;
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hypercalcemia EKG |
shortens QT interval |
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causes of hypomagnesemia?
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GI or renal losses
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impact of hypomagnesemia? |
may cause/increase severity of hypokalemia; may contribute to ventricular arrhythmias w/ acute MI; may potentiate digoxin toxicity, hypocalcemia, Torsades
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causes of hypermagnesemia?
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renal failure or excessive intake
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hypermagnesemia EKG
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no distinct EKG unless severe;
prolonged PR, QRS, cardiac arrest |
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point of hypothermia?
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body temp. below 30 deg. C
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hypothermia EKG |
sinus brady; |
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digitalis effect EKG |
asymmetric ST depression ("scoop" in V5, V6) w/ flattening or inversion of T; normal & predictable
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digitalis effect vs. ischemia on ST? |
digitalis: asymmetric ST depression
ischemia: symmetric ST depression |
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digitalis toxicity causes ... |
sinus node depression; |
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conduction blocks in digitalis toxicity
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slowed conduction through AV node; can cause 1st, 2nd, or 3rd deg. AV block
most common 2nd |
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digitalis vs. BBs
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digitalis useful for SVTs (ex. a-fib), but not good during exertion; BBs have similar effect on AV conduction & may control rate better w/ increased adrenergic tone |
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tachyarrhythmias in digitalis toxicity
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digi enhances auto behavior of all cardiac conducting cells ->
more prone to tachyarrhythmias; esp. PAT & PVCs |
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combinations in digitalis toxicity |
most common: PAT w/ 2nd deg. AV block; usually 2:1 but can vary
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antiarrhythmics that can increase QT interval
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sotalol, quinidine, procainamide, disopyramide, amiodarone; all increase risk for tachyarrhythmias
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When to stop QT-prolongating meds?
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if QT prolongs by >25%
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other meds that can increase QT interval? |
tricyclic antidepressants, phenothiazines, erythromycin, quinolones, antifungal meds |
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Tx for genetically prolonged QT?
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BBs, implantable defibrillators, restricted from competitive sports; cannot take drugs that prolong QT |
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Why & how to calculate the QTc?
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QT interval varies w/ heart rate; equals (QT interval)/(sqrt of R-R interval) |
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QTc limit
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should not exceed 500 ms during therapy (550 ms if underlying BBB) to decrease risk for ventricular arrhythmia |
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QTc is most accurate w/...
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HRs between 50-120 bpm
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conditions w/ ST elevation
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acute injury*, ventricular aneurysm, pericarditis, benign early repolarization, Brugada (v1-V3), athletic hearts (v1-V6) apical ballooning , prinzmetal angina |
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conditions w/ deep T wave inversion
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ischemia, LVH w/ repolarization, BBB, non Qwave infarct, subarachnoid bleed, athletic , digitalis therapeutic, acute PE (lead III only), angina, apical balloon |
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pericarditis EKG |
diffuse ST elevation T wave flattening/inversion no Q waves |
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pericarditis vs MI? |
Pericarditis: ST-T changes diffuse; |
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pericardial effusion
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low voltage in all leads; may cause electrical alternans
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Osborn J wave
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assoc. w/ hypothermia; |
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electrical alternans
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assoc. w/ large pericardial effusion; electrical axis varies w/ each beat; varying amplitudes of each waveform
loss of isoelectric line |
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hypertrophic obstructive cardiomyopathy
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may have LVH, Left axis Deviation, Q waves laterally (& occasionally inferiorly) |
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myocarditis
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can cause conduction blocks, esp. BBBs & hemiblocks
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COPD
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may have low voltage , Right access Deviation, poor R wave progression; p pulmonale
can lead to RHF & show RA enlargement & RVH w/ repol. abnormalities |
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Why low voltage in COPD?
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dampening effects of air trapped in lungs |
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Why Right axis deviate in COPD? |
expanded lungs force heart into vertical or rightward position, & pressure overload hypertrophy from pulmonary HTN
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P pulmonale
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right atrial enlargement; seen in COPD
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acute pulmonary embolism
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usually NSR; can see RVH w/ repol changes due to RV dilatation, poor R wave progression RBBB,
***large S in I, deep Q in III, inverted T in III (S1Q3T3)
sinus tach or afib |
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PE vs. MI EKG? |
in PE, Q wave is only in lead III; in MI, Q waves in at least 2 inf. leads |
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most common arrhythmias in acute PE |
sinus tach & a-fib |
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subarachnoid bleed or cerebral infarction
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diffuse T wave inversion (deep, wide, symmetrical) & prominent U waves
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CNS disease vs. ventricular hypertrophy?
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in CNS disease, T waves are symmetrical; in ventricular hypertrophy, T waves are asymmetrical
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common arrhythmia w/ CNS dysfunction?
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sinus bradycardia
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most common cause of SCD?
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atherosclerosis (CAD) causing infarction or arrhythmia
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commotio cordis
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blunt force to chest causes v-fib (ex. baseball pitcher)
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etiology of Brugada syndrome
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autosomal dom.; more common in 20-30 y/o men; affects voltage dependent sodium channels during repol.
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Brugada syndrome on EKG
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RBBB & ST elevation in V1, V2, V3; can cause ventricular arrhythmias that can cause SCD, esp. in sleep
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Mgmt for Brugada
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implantable defibrillator; all family need screening
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Most common arrhythmia in Brugada?
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fast polymorphic v-tach that looks like Torsades
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Brugada vs regular RBBB?
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typical RBBB doesn't cause ST elevation, but Brugada does
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changes in athlete's heart?
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nonspecific ST-T changes, esp ST elevation in precordial leads w/ T flattening or inversion; LVH, sometimes RVH; arrhythmias, inc. junctional rhythms & WAP; 1st deg or Wenkebach block
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Most common causes of SCD in athletes?
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disorders of heart muscle & sudden ventricular arrhythmias
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troponin
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rises in 2-3 hours; elevated for several days
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CK-MB
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rises in 6 hours; normal within 48 hours
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T wave changes in MI
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hyperacute (peaked) at onset;
a few hours later, invert (ischemia); w/ infarct, inversion persists (months-years) |
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ST elevation in MI looks... |
reversible injury; domed upward; may merge w/ T; reliable sign of MI; normalizes in a few hours |
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J point
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where ST segment takes off from QRS complex; elevation common in athletes (baseline w/ exercise); aka "early repolarization;" T stays independent
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Q waves in MI
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irreversible cell death; diagnostic; appear several hours after onset (ST has returned to baseline already), but may take days to evolve; present for life
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normal Q waves
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small in left lateral leads & sometimes inferior leads; *aVR normally has very deep Q* - do not use aVR to assess for MI
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significant Q waves |
>0.04 sec (one small sq) |
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ideal Tx for acute coronary syndrome
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emergency angioplasty & stent placement |
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RCA |
runs between RA & RV; swings around to post.; in most, gives off descending branch (supplies AV node); |
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LAD artery |
supplies ant. wall & most of interventricular septum |
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left circumflex artery |
runs between LA & LV; supplies lateral wall of left ventricle
implicated in lateral infarcts |
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inferior infarcts |
occlusion of RCA or its descending branch;
For 50% of pts, significant Qs disappear within 6 mo; small Qs may suggest old inf. infarct or be normal |
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lateral infarcts |
left lateral wall; occlusion of LCA; |
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anterior infarcts |
anterior surface of LV; occlusion of LAD changes in V1-V6; (septal infarct = V1, V2)
Qs not always formed; instead poor R wave progression |
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occlusion of left main artery? |
anterolateral infarct; changes in precordial leads & I, aVL (recip = inferior)
widow maker |
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poor R wave progression |
in anterior infarcts, RVH, COPD improper lead placement |
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posterior infarcts |
occlusion of RCA; reciprocal changes (ST depression, tall R) in anterior leads, esp. V1 |
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tall R (>s) wave in V1? |
suggestive of posterior infarct
(unless RAD too - then it's RV hypertrophy) |
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non-Q wave infarctions |
T wave inversion & ST depression (at least 48h); lower initial mortality rate, but higher risk for later infarction & mortality |
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apical ballooning syndrome |
mimics MI; T wave inversion & ST elevation; troponins can be elevated, but no CAD; mostly elderly women |
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angina |
dull, burning, boring substernal heaviness;
If ST depressed for >48 hr, is non-Q MI |
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Prinzmetal's angina |
ST elevation (reversible transmural injury); baseline w/ nitro; not necessarily assoc. w CAD |
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MI in LBBB? |
ST elevated >1 mm in any lead w/ predominant R wave (suggestive of MI) |
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pseudoinfarct pattern |
in WPW, delta waves often neg. in inf. leads; may resemble Q waves; use short PR interval to differentiate |
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CT scanning of heart |
measures degree of atherosclerosis; doesn't reliably predict specific site |
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CT angiography |
intermediate step between stress test & catheterization, but has high dye load |
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stop the stress test when... |
pt can't continue; max HR is reached; Sx occur (esp. dropping BP) significant EKG changes |
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positive stress test result |
ST depression |
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stress test suggestive of CAD |
ST horizontal/downsloping depression >1mm that persists for >0.08 sec |
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stress test indications |
CP in pt w/ normal EKG recent infarction (to assess prognosis) >40 w/ diabetes, PVD, prior MI, or FHx suspect silent ischemia (dyspnea, fatigue, palp) >40 starting exercise program |
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stress test contraindications |
acute systemic illness severe aortic stenosis uncontrolled CHF severe HTN angina at rest significant arrhythmia |
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improving sensitivity/specificity of stress test? |
Echo (before/after; look for wall motion change) radioactive imaging (look for perfusion defect) |
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adenosine stress testing |
causes coronary vasodilation; increases blood flow ~ 400%; diseased vessels have less uptake of tracer typically no diagnostic EKG changes during test |
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dobutamine stress testing |
adrenaline-line agent; mimics stress of exercise; w/ CAD, will see EKG changes & wall motion abnormalities on Echo
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where do you see U waves? |
1)hypokalemia 2) stroke 3) subarachnoid bleed |
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conditions w/ ST depression |
hypokalemia stress test posterior MI digoxin therapeutic non Q wave infarction angina (return after attack) |
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WPW vs LGL EKG |
WPW- delta wave, wide QRS short PR
LGL just short PR |
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WPW vs LGL bundles |
wpw-bundle of kent abherrant
lgl-james fibers intranodal |
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orthodromic vs antidromic |
ortho-normal route anti- backwards through av node |
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common arrhythmia is WPW |
PSVT and afib
can get going really fast=death |
