-
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
-
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
-
which electrolyte disorder?
decreased ST
u wave (comes after T but before next P) PVCs
hypokalemia
-
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)
-
which electrolyte disorder?
bradycardia
wide QRS
ventricular arrhythmias
hypermagnesemia
-
what causes hypermagnesemia?
- from Mg (i.e. antacids, cathartic)
- repeat dose, renal function issue
-
antidote for hypermagenesemia?
IV calcium
-
which electrolyte disorder?
dysrhythmia especially if treated with digoxin
hypomagnesemia
-
which electrolyte disorder?
short QT
occasional depressed ST
sinus arrest
AV block
hypercalcemia
-
which electrolyte disorder?
long QT
some broadening of T
hypocalcemia
-
why does myocardial ischemia happen?
- mismatch btwn myocardial O2 demand and supply
- demand exceeds supply
-
similarity btwn angina and myocardial ischemia
sympts are similar
-
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
-
two mechanisms behind myocardial ischemia
- increased demand (increased heart rate, BP, underlying CAD)
- oxygen supply (coronary blood flow, oxygen carrying capacity of the blood)
-
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
-
during MI, vasoconstriction affects oxygen supply and coronary blood flow. which drugs affect this?
-
during MI, oxygen supply is affected by hypotension. which agents affect this mechanism?
- PDE5 inhibitor + nitrates
- dipyridamole
-
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.
-
antidote for methemoglobin inducers (benzocaine, dapsone)?
methylene blue
-
ruptured plaque and thrombosis of MI is caused by..
-
vasospasm of MI is caused by...
-
how to correct vasospasm (MI) caused by cocaine?
- IV phentolamine
- alpha blocker
-
how to correct ergot-induced vasospasm (MI)?
- IV NTG, IV vasodilator
- (ergot and cocaine cause vasoconstriction)
-
accelerated atherosclerosis of MI is caused by ...
protease inhibitor and cocaine
-
how would you manage MI?
- with CAD: according to guidelines
- without CAD: d/c drug and treat ischemia
-
how does cocaine cause myocardial infarction?
- 1) ruptured plaque = thrombosis
- 2) vasospasm
- 3) accelerated atherosclerosis
-
what should you AVOID acutely in cocaine associated chest pain?
beta blockers b/c causes unopposed alpha and worsens
-
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)
-
how does HF affect the body?
heart fails to pump enough blood to meet the metabolic demand of the body
-
drug induced HF without pre-existing disease is... common or rare?
rare
-
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
-
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
-
agents that exacerbate HF by reducing myocardial contractility?
- acute use of beta blocker
- CCB (diltiazem and verapamil are contraindicated in HF)
- anthracycline
- trastuzumab
-
agents that exacerbate HF by increasing preload?
- glucocorticoids
- glitazones (Actos is dose-dep)
- NSAID
- COX 2 inhibitor
-
agents that exacerbate HF by increasing after load
sympathomimetic due to vasoconstriction
-
2 medication options to treat HF?
-
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
-
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
-
-
normal QRS sec?
<0.12 sec
-
-
P wave signifies what in EKG?
atrial depolarization
-
Q waves signifies what in EKG?
ventricular depolarization
-
T wave signifies what in EKG?
ventricular repolarization
-
in sinus pause/arrest, what happened?
- sinus node is impaired transiently
- thus there are pauses without P wave on EKG
-
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
-
how does AV block occur?
conductino of impulse from atria to ventricle thru the AV node is delayed or inhibited.
-
which degrees of AV block result in bradycardia?
2nd and 3rd degrees
|
|
