Unit 2- concepts Flashcards
(54 cards)
1
Q
aldosterone
A
- released from adrenal cortex in response to high K+ and H+ levels or low Na+ levels
- acts on distal tubules of kidney to cause retention of Na+ and excretion of K+/H+
- Na+ retention leads to water retention -> BP rise
2
Q
aldosterone and Na+/K+ exchange
A
- stimulates reabsorption of Na+ from DCT
* causes K+ to be secreted
3
Q
fxns angiotensin (5)
A
- constricts vessels, increasing vascular resistance
- stimulates aldosterone release from adrenal cortex
- stimulates release of vasopressin (ADH) from pituitary
- facilitates NE release and inhibits re-uptake from nerve endings (-> SNS)
- stimulates cardiac/vascular hypertrophy
4
Q
decrease of angiotensin II results in…
A
•vasodilation •decreased blood volume •decreased cardiac/vascular remodeling •K+ retention •fetal injury *accomplished by ACE inhibs
5
Q
first dose hypertension
A
- orthostatic hypotension after the first dose of BP medication
- often results in syncope
- common with ACE inhibs
- can be avoided by taking the first dose at night
6
Q
reflex tachycardia
A
- in response to decreased blood volume the heart beats faster in attempts to raise it
- causes include orthostatic hypotension, meds, and FVD
- avoided by combining anti-HTN w/ beta blocker
7
Q
myocardial infarction (MI)
A
•occurs when artery is completely occluded
8
Q
angina pectoris
A
- chest pain due to CAD and myocardial ischemia
- result of imbalance b/t myocardial O2 supply and demand
- tx to prevent MI, pain, etc
9
Q
exertional angina
A
•angina (pain) occurs durning physical exertion/stress
10
Q
vasospastic angina
A
- may occur at any time
* due to coronary artery vasospasm
11
Q
untreated CAD and angina may lead to…
A
- MI
* death
12
Q
nitric oxide
A
•potent vasodilator of blood
13
Q
heart failure
A
- weakening of contractile fxn of heart
- blood/fld accum. in heart, lungs, abdomen, and lower extremities
- dec. CO and BP unable to meet body’s O2 needs
14
Q
cardiovascular reflexes for CHF
A
- vasoconstriction
- tachycardia
- Na+/H2O retention
15
Q
s/s CHF
A
- dec. tissue perfusion- weak/activity intolerance
- L side- pulmonary congestion
- R side- systemic congestion
16
Q
dromotropic effects on heart
A
- inc. SPEED of ctx
* - dec. SPEED of ctx
17
Q
inotropic effects on heart
A
- inc. FORCE of ctx
* - dec FORCE of ctx
18
Q
chronotropic effects on heart
A
- inc. SA HR
* - dec. SA HR
19
Q
angioedema
A
•swelling affecting deeper layers of skin
•most common around eyes and lips
*hives under skin
20
Q
goal of dysrhythmia tx
A
•keep HR b/t 60 and 100 bpm
21
Q
what does HR have to be to admin dig
A
•60 bpm
22
Q
important before admin/taking cardiac drugs
A
•take BP and HR
23
Q
CCB for angina pectoris
A
•decreases myocardial contractility
24
Q
CCB for HTN
A
•relaxes smooth muscle
25
CCB for dysrhythmia
•slows HR and AV conduction
26
CCB interaction w/ Quinidine, carbamazepine, cyclosporine
* inhibits their metabolism
| * leads to toxicity
27
best HDL raising drug
* Nicotinic acid (Niacor)
| * Niacin (Niaspan)
28
very low density lipoproteins (VLDLs)
•triglycerides
29
low density lipoproteins (LDLs)
* bad
* contribute to atherosclerosis
* levels should be less than 100 mg/dL
30
high density lipoproteins (HDLs)
* good
* prevent atherosclerosis
* levels should be greater than 40 mg/dL
31
important about fibrates
•reduce levels of TGs, not LDLs
32
class I medications
* sodium-channel blockers
| * slow conduction
33
class II medications
* beta blockers
| * prevent SNS stimulation of heart
34
class III medications
* K+ channel blockers
| * prolong refractory period
35
class IV medications
* CCBs
* decrease force of ctxn
* relax smooth muscle
* decrease HR and AV conduction
36
A client with hypertension is receiving furosemide (Lasix). Which data indicates the medication is effective?
8-hour intake is 1800 ml and output is 2300ml
37
A client with essential hypertension is prescribed hydrochlorothiazide (Diuril). The nurse should provide this information to the client
drink adequate amounts of fluid
38
contraindications for Lasix or HCTZ
* pregnancy
* lactation
* diabetes
* hypokalemia
39
digoxin (Lanoxin) and furosemide (Lasix) interaction
•ventricular dysrhythmias in presence of hypokalemia
•Dig is very dependent on K+, so will get dig toxicity
*K+ sparing agents often admin to prevent
*monitor heart and K+ levels
40
primary reason to stop ACEI therapy
•cough
41
digoxin effect time
* t1/2: 1.5 days
* plateauL 6 days
* oral effects: 30 min- 2 hr
* peak: 4-6 hrs
42
halo effect with digoxin use
•visual disturbance indicating overdose
43
digoxin toxicity tx
* stop drug
* treat cause
* treat dysrhythmia
* admin Digoxin Immune FAB (digibind)
44
positive inotropic effect of digoxin
•increase contractile force of myocardial ctx
| -results in improved SC and CO
45
negative chronotropic effect of digoxin
•decreased HR-
- results in more time for ventricular filling
- results in increased SV and CO
46
hyperkalemia and cardiac glycoside interaction
•decreases actions of cardiac glycoside
47
hypercalcemia and cardiac glycoside interactions
•increases actions and toxicity of cardiac glycosides
48
digoxin dosing
* initial digitalization doses to rapidly attain effective therapeutic concentration
* lower daily doses given to maintain therapeutic concentrations
49
digitalization
* using loading dose to achieve therapeutic levels quickly
* usually 4 divided dose of 0.25 mg
* admin PO or slow IV push (5 min)
50
digoxin maintenance
•adults 0.125-0.5 mg/day
•typical is 0.25 mg/day
*HR MUST be above 60 and stable BP before admin
51
digoxin therapeutic plasma levels
•0.5-2.0 ng/mL
52
diuretic therapy for CHF
* eliminates excess Na/fld
* results in more effective heart fxn
* can be used in combo w/ cardiac glycosides and other drugs, but monitor K+
53
vasodilator therapy for CHF
•relax/dilate blood vessels
•decreases peripheral resistance, allowing more efficient blood flow
*most common are ACEIs and ARBs
54
Phosphodiesterase inhibitors
* amrinone; milrinone
* short term IV therapy for CHF
* positive inotropic agents w/ vasodilator properties
* increase myocardial contractility
