physiology of the heart Flashcards

(60 cards)

1
Q

what is a U wave

A

this is purkinje repolarization after the T wave. due to hypokalemia

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2
Q

J wave

A

this is a separate wave within the ST segment that has to due with hypothermia or hypocalcemia.

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3
Q

when to use thiazides

A

moderate to mild HTN. since they are in the middle for potentcy

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4
Q

when to use loops

A

HTN crisis, CHF, cirrhosis, renal dysfucntion

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5
Q

what to watch out for with diuretics

A

HSR to thiazides, volume depletion, hypokalemia, hypomagnesemia, glucose intolerance, lipid profile, ototoxic, erectile dysfunction,

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6
Q

caution for potassium sparing

A

gynecomastia in men, breast pain, menstrual irregularities, hyperkalemia. do not use in renal failure, diabetes, or when using ACEi and ARBs.

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7
Q

list of potassium sparing diuretics

A

amiloride, triemterine, spironolactone.

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8
Q

mechanism of ACEi

A

blocks ACE from converting angiotensin I to angiotensin II also inhibits the breakdown of bradykinin.

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9
Q

mechanism for ARBS

A

inhibits angiotensin II from binding to its receptor and stops the release of aldosterone and vasodilator

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10
Q

side effects of ACEi and ARBs

A

cough (not ARBs), hypotension, decreased renal function, angioedema.

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11
Q

when are ACEi and ARBs contraindicatred

A

renal artery stenosis, hyperkalemia, caution in renal failure, pregnancy

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12
Q

what else do ACEi and ARBs do?

A

benefit chronic renal failure (NOT ACUTE) congestive HF, LV remodeling, LVH, may even reduce risk of diabetes.

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13
Q

what do CCBs do?

A

they inhibit the Ca influx for vascular sooth muscle thus decrease TPR.

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14
Q

what are the two classes of CCBs

A

dihyropyridines and non dipine

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15
Q

what are the two dipine used

A

amlodipine and nifedipine

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16
Q

what are the two nondipines

A

diltiazem and verapamil

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17
Q

what else to CCB do?

A

good for raynauds, antianginal

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18
Q

when treating angina with dipine what do we watch out for?

A

reflex tachy and worsening angina

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19
Q

what is the main reason to use a beta blocker for HTN

A

to reduce cardiac output.

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20
Q

what secondary reasons do we use b blockers for

A

to decrease the release of renin

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21
Q

side effects for beta blockers

A

decreased exercise tolerance, bronchospasm, bradycardia, CHF due to negative inotropy, mask symptoms of hypoglycemia, depression, worsening PVD

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22
Q

why use metoprolol and atenolol

A

because they have cardiogenic selectivity and not broncho interference. if asthma and need a beta blocker use a selective like metoprolol and atenolol

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23
Q

why use carvedilol, esmolol and labetolol

A

these are used for HTN urgency or acute coronary syndromes. because they have additional sympathomimetic activity and can drastically lower BP.

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24
Q

what is the main use for esmolol

A

AV nodal blocking. it is unique due to its short half life.

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25
alpha blockers mechanism
reduces vascular resistance.
26
aphla blockers examples
terazosin and doxazosin
27
SE of alpha blockers
orthostatic hypertension, fkuid retention, worse angina
28
even though they are clearly outdated, why use alpha blockers at all
because they can aid in BPH
29
examples of systemic vasodilators
hydralazine and minoxidil
30
mechanism of hydralazine and minoxidil
they are vasodilators by relaxing smooth muscle of arterioles
31
when to use hydralazine and minoxidil
in CHF and HTN. also used in refractory HTN.
32
central acting sympathoplegic
these are alpha 2 agonists that reduce sympathetic outflow from the brainstem. the decreased sympathetic tone also reduces release of renin
33
examples of central sympathp
clonidine, methyldopa, guanabenz
34
when to use methyl dopa
during pregnancy
35
SE of the central acting
sedation, dry mouth, rebound HTN. fatigue, orthostatic hypotension, depression.
36
what are ganglion blockers
adrenergic neuron blocking agents. pharma sympathectomy.
37
examples of ganglion blockers? 2
guanethidine and reserpine.
38
SE of the ganglion blockers
sedation, parkinson, mental status changes
39
aspirin uses
CAD.
40
what is aspirin mechanism
irreversible inhibition of COX enzymes. blocking prostaglandin and thromboxane synthesis
41
ticlopidine what is it and when to use it?
this an alternative to aspirin for treating CAD. it is a thienopyridine derivative that inhibits platelet aggregation by ADP. decreases fibrinogen and thus blood viscosity
42
SE of ticlopidine
neutropenia and TTP
43
clopidogrel what is it and when to use it
alternative to aspirin, it is a thienopyridine derivative with a greater anitthrombotic activity than ticlopidine. selectively inhbits the ADP platelet receptor.
44
prasugrel what is it and when
this is another anti platelet alternative to aspirin. same family.
45
who can we use prasugrel on?
<75 years of age, greater than 60kg, no history of stroke of TIA
46
dipyridamole
pyrimido-pyrimidine derivative. increases cAMP inhibits PDE, activates adenylyl cyclase limited use due to exercise induced ischemia
47
cilostazol
another alternative to aspirin for anti platelet. quinilone derivative that inhibits PDE. increases cAMP leading to inhibition of platelet aggregation.
48
which beta blockers do we use in CAD
beta 1 selective or cardioselective
49
which are beta 1 selective
metoprolol, atenolol, bisoprolol
50
when not to use Beta blockers
bradycardia, AV block, sick sinus syndrome, unstable LVF, asthma, severe depression, peripheral vascular disease.
51
SE of beta
sedation, fatigue, decreased exercise tolerance. lethargy, insomnia, claudication worse, impotence
52
contra for nitrates
hypotension, aortic stenosis, hypertrophic cardiomyopathy, use of PDE to treat erectile dysfunction
53
SE to nitrates
tolerance. HA, hypotension.
54
digoxin when to use it
use for HF. it stimulates the heart.
55
what is the mechanism for digoxin
it inhibits the Na/k ATPase. this allows for calcium to come into the heart cell giving the heart an increased force of contraction due to the calcium.
56
what does digoxin do for the heart in CHF?
it increases CO, LVEF, exercise tolerance, natriuresis, vagal tone, and decreases LVEDP, NE, RAAS, and neural-hormonal activity.
57
why is use of digoxin waining
due to the narrow therapeutic window. can be toxic and proarrhthmigenic
58
what is dobutamine and when do we use it
we use it in heart failure. it is a direct beta agonist
59
what are the downfalls od dobutamine
tolerance develops within 48 hrs.
60
what is milrinone and when do we use it
it is a PDEi that increases contractility and relaxation. we use it in HF. there is no tolerance up to 72 hours.