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NUR 326 > module 4 > Flashcards

module 4 Flashcards

1
Q

what are the two main determinants of blood pressure

A

cardiac output and peripheral vascular resistance

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2
Q

preload and afterload

A

the preload is the amount of blood in the heart prior to contraction at the end of diastole. The stretching of the sarcomeres. the afterload is the for against which the heart must squeeze to eject the blood. this is the resistance the heart must overcome to open the aortic valve

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3
Q

Cardiac output calculation

A

stroke volume times the HR. should be 4-8L per minute

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4
Q

contractility

A

the strength at which the heart contracts during systole

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5
Q

autroregulation of BP

A
  • the kidneys help to control the volume of fluid
  • the RAAS is a series or hormonal mechanisms that control BP through elimination and retentions of of sodium and water
  • the endothelial cells that line blood vessels regulate vasodilation, vasoconstriction and vascular tone.
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6
Q

RAAS

A
  1. decreased perfusion pressure (low BP) stimulates the secretion of renin by the juxtaglomerular cells in the kidneys
  2. renin converts angiotensinogen which is produced in the liver to angiotensin I
  3. angiotensin I is converted to angiotensin II by the angiotensin-converting enzyme (ACE) found in the pulmonary capillary beds
  4. angiotensin II is a powerful vasoconstrictor causing increased BP
  5. Angiotensin II also stimulates the release of the hormone aldosterone from the adrenal cortex
  6. Aldosterone causes increased sodium and water reabsorption by the tubules of the kidney which results in increased blood pressure
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7
Q

beta adrenergic receptors

A

neural regulation of blood pressure mainly involves the sympathetic nervous system. This system stimulates beta-adrenergic receptors in the heart which increase HR and force of myocardial contraction.

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8
Q

ACE inhibitors increase the risk of

A

cough, hyperkalemia, angioedema, and fetal death.

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9
Q

examples of ACE inhibitors

A

captopril = Capoten
enalapril maleate = (vastec)
lisinopril (prinivil or zestril)
it is recommended that ACE inhibitors be used as first-line agents for treating hypertension, particularly in patients with HF

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10
Q

captopril

A

Capoten. it may increase serum concentrations of digoxin and lithium and increase the risk of elevated serum levels which can lead to toxicity. take 1 hour before a meal

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11
Q

lisinopril

A

Prinivil or Zestril
is indicated for the treatment of hypertension and HF. in the case of an MI this med can be used adjunctively with other drugs. (together)

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12
Q

angioedema

A

an adverse reaction of an ACE inhibitor.

sudden swelling or welts under the skin, common areas include the eyes, lips, and tongue

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13
Q

neutropenia

A

a serious complication of captopril in which the # of neutrophils is diminished. check the CBC for this

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14
Q

side effects of ACE inhibitors

A 
irritating dry cough
insomina
hyperkalemia
tachycardia
NV
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15
Q

contraindications and BB for ACE inhibitors

A

BB: if used in pregnancy there is death to the fetus
contraindications: potassium sparing diuretics such as spironolactone (aldactone) and salt substances that contain potassium

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16
Q

angiotensin II receptor blockers (ARBs) examples

A 
losartan = cozier
Valsartan = diovan
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17
Q

ARBs BB warning

A

pregnancy bc it can cause death to the fetus

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18
Q

examples of Calcium channel blockers

A 
amiodipine = norvasc
nifedipine = procardia
ditiazem = cardizem
verapamil = Calan SR
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19
Q

amiodipine

A

norvasc:

do not take with St. johns wart because it may decrease the affect of the drug

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20
Q

nifedipine

A

procardia:
do not take this with grapefruit juice because it increases the effects of the drug causing excessive vasodilation, hypotension, dizziness, and headache.
should not abruptly stop taking this drug because it can result in rebound tachycardia

21
Q

diltiazem

A

Cardizem

monitor for dysrhythmias, AV heart block, bradycardia, HF, htn, headache and dizziness

22
Q

verapamil

A

Calan SR:
do not split or crush extended-release or take with grapefruit juice. monitor for excessive vasodilation, hypotension dizziness, and headache

23
Q

Direct Renin inhibitor example

A

aliskiren = Tekturna
this is the only direct renin inhibitor. it decreases the plasma renin activity which inhibits the RAAS cascade
can be taken by itself or with other antihypertensives but NEVER with ACE inhibitors or ARBs because that will kill the kidneys

24
Q

Beta blockers examples

A 
Atenolol (Tenormin) 
Esmolol  (Brevibloc)
Metoprolol (Lopressor)
Propranolol (Inderal) 
Metoprolol succinate (Toprol-XL) long acting
25
Q

what does blocking beta I receptors in the heart do?

A

decreases the HR so this is a negative chronotropic effect
ex: propranolol which is the stage fright drug

decrease myocardial contractility so have a negative inotropic effect ex: lidocaine

decrease rate of conduction fro SA to AV node having a negative dromotropic effect
exL: verapamil

26
Q

what is a positive chronotropic effect

A

increaseing the HR and stimulating the SNS for ex:F norepinephrine or levophed

27
Q

what is a positive inotropic effect

A

meds that increase myocardial contraction like digoxin

28
Q

what is a positive dromotroic effect

A

increases the rate at which there is condition from SA to AV

ex: mexiletine

29
Q

cardio selective beta If blockers

A

act on the heart alone

  • metoprolol (loperessor)
  • atenolol (tenormin)
  • esmolol (brevibloc)
30
Q

nonselective beta blockers

A

BEta I and BEta II
propranolol (Inderal)
act everywhere so thing stage right you want no sweat, bronchioles dilated and decrease HR

31
Q

alpha and beta clockers

A

carveilol (coreg)

labetalol (trandate)

32
Q

BB for beta blockers

A

those with CAD on oral BB and go through abrupt withdrawal have seen an exacerbation of angina vent arrhythmias and MI

33
Q

vasodilators

A

used in severe hypertension that is not responding to other medications. it acts directly on smooth muscle causing vasodilation, decr BP. does not inhibit renin and does not limit tachycardia
can reduce the afterload and is usually used in the ICU. levels of this drug need to be measured if taken for more than 72 hours and vitals are recycled every 5-15 mins

34
Q

examples of vasodilators

A

Nitroprusside ( IV )

Nitroglycerine (IV)

35
Q

thiazide diuretics

A

hydrochlorothiazide = Microzide
chlorothiazide= diuril
this is the most common diuretic for htn and is used in the distal convoluted tubule to treat mild to moderate htn and edema associated with HF.
-Effect glucose tolerance so caution with diabetes
Not recommended for patients with renal insufficiency because there must be an adequate flow of urine to use this diuretic

36
Q

loop diuretics

A

furosemide (lasix)

  • loop diuretic located in the loop of henle
  • used to treat htn and peripheral edema
  • used for pt with renal insufficiency. they typically are anuric and are dialysed
  • does not depress renal blood flow
  • Not used if hypertension is the result of rennin-angiotensin-aldosterone system because they tend to increase renin level
37
Q

potassium sparing diuretics

A

spironolactone (Aldactone) blocks aldosterone receptors in the kidney resulting in the excretion of NA and H2O
-located in the collecting duct
-used as mild diuretics in combination with other diuretics for HF
-also not used for pt with renal insufficiency
potassium-sparing so check levels of k
-used for patients who are at risk for hypokalemia

38
Q

stages of HF

A

stage 1 is considered a high risk for HF without symptoms or structural disease
stage 4 is considered severe structural heart disease and marked symptoms of HF at rest

39
Q

natriuretic peptides

A

a foamily of related hormones that help maintain sodium and fluid balance. the most common peptides peptides are ANP and BNP. in HF circulating levels of BNP rise and signifying ventricular dilation.

40
Q

ANH

A

atrial natriuretic hormone
normal value is 20-77 pg/ml or 20-77 ng/L
elevation HF

41
Q

BNP

A

brain natriuretic peptide
a normal value less than 100pg/L
assist with differentiation of lung disease

42
Q

Digitalis

A

this medication inhibits the sodium-potassium pumps leading to increased intracellular sodium leading to an influx of calcium causing stronger contraction or more efficient contraction.
The Increase in contraction results in peripheral and kidney function enhances cardiac output, decreases preload, improves blood flow to the periphery and kidneys, decreases edema and promotes fluid excretion

43
Q

digoxin

A

a cardiac glycoside. similar to digitalis but it is the manmade version
Increase force and velocity of myocardial systolic contraction
Slows heart rate
Used to treat Atrial fibrillation and Atrial flutter

44
Q

therapeutic level of dig

A

0.5-2ng/ml
Treat HF lower therapeutic level
Treat A Fib Higher therapeutic level

45
Q

cautions of digoxin

A

Caution with renal patients they should be on digitoxin which is excreted in the liver not the kidneys—digoxin is excreted in the kidneys
-caution with hypo (low levels of dig) and hyperthyroidism (higher levels of dig)

46
Q

side effects of digoxin

A
  • bradycardia
  • N/V/D
  • loss of appetite
  • visual disturbances
  • mental changes
  • headache
47
Q

life threatning effects of digoxin

A

Atrioventricular block
Cardiac dysrhythmias
PVCs
the antidote for dig is digibind which binds with the drug inhibiting it by making complex molecules

48
Q

geriatric implications

A

start with low infrequent does and keep increasing
they are at risk for side effects, adverse reactions
side effects in diuretics are dose dependent so the greater the dose the greater the side effects
-nonpharm methods are used to reduce BP such as exercise, reduction of salt and alc.

NUR 326 (7 decks)

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