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twinklemuse
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which electrolyte disorder?
tall peaked T
decrease P wave
increase PR interval
P is lost
depressed ST
QRS blends into T
sine wave
cardiac arrest
hyperkalemia
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how do you get hyperkalemia? (drugs, conditions)
from potassium salt, K sparing diuretics (spironolactone, triamterene), increased K+ (ACEi), acute OD of digoxin esp in decreased renal fxn, NSAID
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which electrolyte disorder?
decreased ST
u wave (comes after T but before next P) PVCs
hypokalemia
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what are the causes of hypokalemia?
- diuretics (esp. loop)
- vomiting
- ingestion of magic shave (b/c contains soluble barium salt that drives potassium into cells --> profound hypokalemia)
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which electrolyte disorder?
bradycardia
wide QRS
ventricular arrhythmias
hypermagnesemia
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what causes hypermagnesemia?
- from Mg (i.e. antacids, cathartic)
- repeat dose, renal function issue
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antidote for hypermagenesemia?
IV calcium
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which electrolyte disorder?
dysrhythmia especially if treated with digoxin
hypomagnesemia
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which electrolyte disorder?
short QT
occasional depressed ST
sinus arrest
AV block
hypercalcemia
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which electrolyte disorder?
long QT
some broadening of T
hypocalcemia
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why does myocardial ischemia happen?
- mismatch btwn myocardial O2 demand and supply
- demand exceeds supply
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similarity btwn angina and myocardial ischemia
sympts are similar
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difference btwn myocardial ischemia and angina
- MI: oxygen supply is decreased due to clots (use fibrinolytics and thrombolytics), "supply" issue
- angina: chronic exertinal angina, "demand" issue, use NTG to relieve
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two mechanisms behind myocardial ischemia
- increased demand (increased heart rate, BP, underlying CAD)
- oxygen supply (coronary blood flow, oxygen carrying capacity of the blood)
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during MI, there is increased HR and BP due to increased demand. which drugs cause this?
- sympathomimetics (einephrine, cocaine)
- abrupt d/c of BB and central a-agonist
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during MI, vasoconstriction affects oxygen supply and coronary blood flow. which drugs affect this?
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during MI, oxygen supply is affected by hypotension. which agents affect this mechanism?
- PDE5 inhibitor + nitrates
- dipyridamole
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during MI, oxygen supply is affected by oxygen carrying capacity of blood. which agents affect this mechanism?
- methemoglobin inducers (benzocaine, dapsone)
- Fe3+, not Fe2+, thus cannot carry O2 and decreased O2 supply.
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antidote for methemoglobin inducers (benzocaine, dapsone)?
methylene blue
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ruptured plaque and thrombosis of MI is caused by..
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vasospasm of MI is caused by...
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how to correct vasospasm (MI) caused by cocaine?
- IV phentolamine
- alpha blocker
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how to correct ergot-induced vasospasm (MI)?
- IV NTG, IV vasodilator
- (ergot and cocaine cause vasoconstriction)
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accelerated atherosclerosis of MI is caused by ...
protease inhibitor and cocaine
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how would you manage MI?
- with CAD: according to guidelines
- without CAD: d/c drug and treat ischemia
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how does cocaine cause myocardial infarction?
- 1) ruptured plaque = thrombosis
- 2) vasospasm
- 3) accelerated atherosclerosis
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what should you AVOID acutely in cocaine associated chest pain?
beta blockers b/c causes unopposed alpha and worsens
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how to manage cocaine associated chest pain?
- 1) ASA and benzo (central cooling)
- 2) IV NTG, nitroprusside for persistent htn (IV pentolamine)
- 3) high risk vs. low risk
- 4) if high risk: avoid BB acutely; antiplatelet/antithromb tx
- 5) discharge - ASA, clopidogrel, statin, ACEi (chronic BB if high risk like systolic dysfx, dysrhythmia)
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how does HF affect the body?
heart fails to pump enough blood to meet the metabolic demand of the body
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drug induced HF without pre-existing disease is... common or rare?
rare
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what are two types of HF?
- systolic HF: <40% EF (amount that is squeezed out)
- diastolic HF: EF is fine but stiff left ventricle so cannot be filled with blood
- both have problem pumping blood
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risk factors for HF
- pre-existng LV dysfxn
- history of MI
- CAD
- HTN
- LVH
- aortic or mitral valve disease
- >70 yo
- pre-existing edema
- chronic kidney disease
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agents that exacerbate HF by reducing myocardial contractility?
- acute use of beta blocker
- CCB (diltiazem and verapamil are contraindicated in HF)
- anthracycline
- trastuzumab
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agents that exacerbate HF by increasing preload?
- glucocorticoids
- glitazones (Actos is dose-dep)
- NSAID
- COX 2 inhibitor
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agents that exacerbate HF by increasing after load
sympathomimetic due to vasoconstriction
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2 medication options to treat HF?
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risk factors for doxorubicin induced CHF?
- cumulative dose >550mg/m2
- cumulative dose >400mg/m2 if prior mediastinal radiation, >70yo or <15yo, or prior anthracycline
- concurrent use of other chemo
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how to prevent doxorubicin related cardiac toxicity?
- dexrazoxane (esp if doxo >300mg/m2; may decrease dox efficacy)
- questionable: coQ10, carnitine, pretreat with antihistamines, cromolyn sodium, probucol
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normal QRS sec?
<0.12 sec
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P wave signifies what in EKG?
atrial depolarization
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Q waves signifies what in EKG?
ventricular depolarization
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T wave signifies what in EKG?
ventricular repolarization
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in sinus pause/arrest, what happened?
- sinus node is impaired transiently
- thus there are pauses without P wave on EKG
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what is an important clinical feature in sinus bradycardia, sinus pause and sinus arrest?
HR is low to cannot pump enough blood with oxygen thus leading to dizziness
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how does AV block occur?
conductino of impulse from atria to ventricle thru the AV node is delayed or inhibited.
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which degrees of AV block result in bradycardia?
2nd and 3rd degrees
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