Lecture 4 Flashcards
1
Q
Review anatomy of heart
A
vena cava –> right atria –> tricuspid –> Right ventricle –> Pulmonary valve –> pulmonary artery –> lungs/gets oxygen –> pulmonary veins –> left atria –> mitral valve - left ventricle –> aortic valve –> aorta –> coronary arteries
2
Q
Electrical activity originates from… (3)
A
SA node (natural pacemaker)
AV node
Purkinjie fibers
3
Q
Inside a cardiac cell there is a ___ charge because….
A
there exists a negative charge because of the high K+ and low Na+ and Ca2+ on the inside of the cell as compared to the outside.
4
Q
The ____ automatically builds up an electrical charge about _____ times per minute
A
SA node & 60 - 100
5
Q
Electrical phases & cardiac muscle contraction
–> Phase 0
A
electrical charge starts to build
fast channels for sodium open
Na+ comes into the cell quickly
The faster the influx, the faster the electrical impulse
6
Q
Phase 1
A
When the fast channels close
The electrical changes start to occur
7
Q
Phase 2
A
- When the slow channels for Ca2+ are open
- This is a slow process that causes the electrical impulse to plateau
- Ca2+ is necessary for any muscle contraction
- After the peak of the electrical impulse, K+ ions leave the cell. They are “pushed out”.
8
Q
Phase 3
A
- Ca2+ channels close
- The Na+/K+ pump brings the K+ back in and pushes the Na+ out
- Sodium stabilizes the cell to its resting membrane potential
9
Q
Phase 4
A
- Polarized state is reestablished or repolarized to the baseline state
- Ready to start over
- Entire process took about 400 milliseconds
- Any abnormality in any of this will cause a dysrhythmia
10
Q
Congestive heart failure…What is it?
A
A condition where the heart is unable to pump the blood that arrives at the heart
11
Q
What is CHF caused by?
A
- Myocardial infarction
- Age
- valve problems
- coronary artery disease
12
Q
Does CHF hurt like an MI?
A
No. Painful, but different.
13
Q
If the heart can’t pump enough blood…Kidneys:
A
Build up of waste in blood
14
Q
If the heart can’t pump enough blood…brain
A
disorientation/lack of concentrating
15
Q
If the heart can’t pump enough blood…Lungs
A
SOB, gasping on exertion, drowning in own fluid
16
Q
If the heart can’t pump enough blood…cells
A
slowing of cellular processes
17
Q
If the heart can’t pump enough blood…heart muscle
A
poorer and poorer pumping
18
Q
hearts reaction to lack of blood in vital organs is to _________ to try to pump faster and “keep up”
A
increase HR
19
Q
As the cardiac muscles get less rest between beats, the ___ & ___ are lost from the cells, then…
A
Na+ & Ca2+
then eventually there are no effective beats as this issue compounds on itself to get worse
20
Q
Cardiac Glycosides act by:
A
Inhibiting the Na+/K+ pump and increasing the sodium and calcium in the myocardial cells. Which slows and strengthens the heart’s pumping ability.
(affects phase 3)
21
Q
Positive inotropic effect
A
Increased force of the contraction
22
Q
Negative Chronotropic effect
A
decreases heart rate
23
Q
Negative Dromotropic effect
A
Delays impulse from SA node to AV node
24
Q
Once cardiac glycosides are taken…
A
- Decrease in waste buildup
- Increased mental alertness
- Better breathing
- Better oxygen to cells
- More blood to heart muscle itself
25
Side effects of cardiac glycosides
- very narrow therapeutic level
- easy to become toxic
- requires constant monitoring of blood levels
- women complain of SEVERE vaginal dryness (K jelly)
26
S/S of toxicity cardiac glycosides
1. arrhythmia
2. GI upset/diarrhea
3. change in vision (yellow halo around lights); very late sign
4. headache
5. high K+ level (monitor!!)
27
medication to counter cardiac glycoside toxicity
Digibind
28
cardiac glycosides are the main treatment for...
CHF
29
Digoxin (Lanoxin)
cardiac glycoside
- very strong action
- very narrow therapeutic window
30
nursing considerations for cardiac glycosides
1. take apical pulse for full 60 s
2. ensure good perfusion -- do not give Digoxin if HR < 60; not mentating; low BP; not urinating
3. do not switch brands, miss or double a dose
4. don't give with antacids or milk (decreases action)
31
IRL consideration vs NCLEX consideration of grapefruit juice and Digoxin (cardiac glycosides)
IRL: do not give with grapefruit juice
on NCLEX: it's fine to give with grapefruit juice
(research is conflicting; IRL, err on the side of caution)
32
Antidysrhythmic agents are given to patients with...
slow, fast, or otherwise irregular rhythms
33
class 1 antidysrhythmics
"membrane stabilizing agents"
34
effect of Class 1 Membrane Stabilizing Agents (phase it affects and how)
- slows electrical conduction of the heart by blocking fast Na+ channels
- prolongs Phase 0
35
when to use membrane stabilizing agents
- fast heart conduction problems
| - when AV node is not communicating with SA node
36
what do membrane stabilizing agents treat
tachycardia, fibrillation, premature ventricular contractions
37
membrane stabilizing agents S/E (side effects)
- stomach upset
- headache
- dizziness
- blurred vision
38
S/S of membrane stabilizing agent toxicity
exaggerated action of the desired effect (bradycardia, hypotension, cardiac arrest)
39
interactions of membrane stabilizing agents
grapefruit juice and Quinidine (DO NOT MIX) and Warfarin (thrombolitic -- monitor levels)
40
specific membrane stabilizing agents to remember
Quinidine (PO) and Lidocaine (IV)
both decrease cells' sensitivity to impulses
41
class 2 of antidysrhythmic agents
beta-blockers
42
beta-blocker effects
- blocks sympathetic nervous system stimulation of the heart (blocks beta1 and beta2 receptor sites in heart and lungs)
- prevents catecholamine stimulation of the heart
- makes heart harder to stimulate out of phase 4 (resting phase)
43
catecholamine
epinephrine and norepinephrine
44
effects of beta-blockers
- negative chronotropic effect
| - negative dromotropic effect
45
beta-blockers also treat...
- HTN
| - chest pain
46
Propranolol (Inderal)
beta-blocker medication (note "olol" ending)
47
class 3 of antidysrhythmic medications
no specific name
48
class 3 effects
decrease excitability of the heart -- blocks the reeptors of the sympathetic nervous system
49
class 3 uses
very effective with ventricular tachycardia and some atrial tachycardia
50
class 3 cautions (side effects)
have many side effects...
- can harm the thyroid gland, vision, and alveoli
- long half-life; side effects take a long time to go away
51
Amiodarone
```
class 3 cardiac glycoside medication
(PO and IV)
```
52
corvert (ibutilide)
class 3 cardiac glycoside
- chemical cardioverter
- immediate change in HR
- MD should be present before administering
- can't be given within 4 hrs of Class 1 or Class 3 meds
53
class 4 medications
calcium channel blockers
54
calcium channel blocker effects (phase and what part of the heart it affects)
- slow the inward flow of Ca2+ ions into atria and AV node
- no effect on ventricles
- works primarily on phase 2
55
calcium channel blockers uses
- treat atrial flutter and fibrillation
| - also used to treat HTN and chest pain
56
calcium channel blockers side effect
decreased blood psi
57
calcium channel blocker medications to remember
Verapamil (Calan)
Diltiazem (Cardizem)
58
Important info for all antidysrhythmic meds
- do not miss or double dose
- check pulse; do not admin if <60
- watch for signs of v. low BP
- monitor INR levels
59
Chest pain/angina is caused by...
ischemia to the heart muscle
60
physiology behind angina
1) atherosclerotic plaques in coronary arteries (usually no pain until 70-90% clogged)
2) spasm of coronary arteries (irritated walls "pinch" together)
buildup of plaques or recurrent spasm leads to lack of O2 and nutrients for the heart to pump adequately
61
3 classifications of medications used to treat chest pain
1. nitrates (anti-anginal)
2. beta blockers
3. calcium channel blockers
62
Nitrates effects
- dilates all blood vessels, but primarily coronary arteries
| - pools blood in venous system (takes work off heart, increases blood flow to myocardium
63
S/E of nitrates
- increased HR
- decreased B/P
- HA (common)
- flushing
- dizziness
64
contraindication of nitrates
do not take with ED meds (both drop BP)
65
Nitroglycerin
nitrate
- cannot be taken PO (destroyed by liver)
- sublingually for angina attacks
- IV and spray options
- long term -- patch or paste on skin changed q24h
- monitor BP
66
beta blockers (chest pain version) effects
- slows HR, decreases contractility
- decreases oxygen demand and helps conserve energy of heart muscle
- blocks beta receptors of the heart so catecholamines cannot stimulate the heart
67
s/e of beta blockers (chest pain)
- fatigue and lethargy
- constipation
- depression
(mostly in elderly; admin at bedtime to avoid these)
68
why should you monitor diabetics taking beta blockers?
may mask tachycardia associated w low blood sugar
69
contraindications for beta blockers
- asthma (narrows bronchioles)
- CHF (exceptions - carvedidol and metoprolol XL)
- avoid abrupt discontinuation of beta blockers
70
what else are beta blockers used to treat?
HTN, chest pain, and helping the heart rest after MI
71
beta blocker meds for angina
Metoprolol (lopressor)
| Atenolol (tenormin)
72
calcium channel blockers effects for angina
- reduces cardiac contractility
- dilates peripheral arteries (Relaxing smooth muscle)
- esp effective on coronary artery soasms
73
calcium channel blockers are also used for the treatment of...
HTN and migraine HAs
74
calcium channel med for angina
Nifedipine (v. rapid fx on BP)! often given sublingually
75
HTN
BP of over 140/90 for a prolonged period of time
76
pre-hypertension
120-140/80-90 (start getting treatment before heart damage)
77
formula for bp
cardiac output x systemic vascular resistance = blood pressure
78
types of hypertension
1. essential/primary HTN (no known cause)
| 2. secondary HTN (cause known; e.g. renal, pregnancy)
79
6 categories of antihypertensives
1. beta-blockers
2. calcium channel blockers
3. centrally acting adrenergic agents
4. angiotensin-converting enzyme inhibitors (ACE inhibitors)
5. angiotensin II receptor blockers (ARBs)
6. diuretics
80
centrally acting adrenergic agent actions
- decrease stimulation by the sympathetic nervous system
- work by stimulating alpha2 receptros which...
a) negative chronotropic
b) negative inotropic
c) dilating blood vessels
d) stopping secretion of renin
81
renin
potent vasoconstrictor made by kidneys; increases vascular resistance
82
S/E of centrally acting adrenergic agents
bradycardia
| orthostatic hypotension
83
clonidine (catapress)
centrally acting adrenergic agent
| PO, patch
84
ACE inhibitors effects
- inhibits angiotensin converting enzyme of kidneys
- this blocks production of angiotension II (vasoconstrictor) and aldosterone (retains H2O and Na+)
- decreases afterload (decreasing vascular resistance)
- decreases preload (decreasing blood volume)
85
ACE inhibitors S/E
- dry cough (most common; irritating but not lethal)
- hypotension
- dizziness
- avoid high levels of potassium -- monitor
86
ACE inhibitors examples
Captopril (capoten)
| Enalapril (vasotec)
87
ARBs effect
- blocks action of angiotensin (can still be formed even if ACE inhibitors are used)
- affects smooth muscle and adrenal glands
- block vasoconstriction and aldosterone secretion
88
ARBs S/E
URI (upper respiratory infection) and HAs (headaches)
hypotension
monitor potassium levels
89
ARB medication
Losartan (Cozaar)
| - does not cause dry irritating cough
90
diuretics
accelerate urine formating by stimulating the nephron
91
types of diuretics
a) loop diuretics
b) osmotic diuretics
c) potassium sparing diuretics
d) thiazides
92
loop diuretic actions
- block Na+ and Cl- absorption at loop of Henle
- this decreases the vascular volume
- works rapidly and strongly or about 2 hrs
- wastes potassium and can cause dehydration;
- can also cause permanent deafness; give <10mg/min if giving IV push (ICU)
93
loop diuretic uses
- decreases edema
- help with CHF
- control HTN
94
loop diuretic example
Furosemide (Lasix)
95
osmotic diuretic actions
- inhibit reabsorption of water and solutes; causes reapid diuresis
- wastes electrolytes and can cause dehydration
96
osmotic diuretic uses
- increase excretion of toxic substances (OD)
| - reduce intracranial psi and cerebral edema
97
osmotic diuretic example
Osmitrol (Mannitol)
98
Potassium sparing diuretic actions
- excrete Na+ and H2O, but retains K+
| - weak overall diuretic, but can be used when there is concern about K+ availability to the heart
99
potassium sparing diuretic example
Spironolactone (Aldactone)
100
thiazides action
- loss of H2O, Cl-, Na+, K+
- not good to take if renal blood flow poor
- can cause electrolyte deficiencies
- very inexpensive, often used in combo w other diuretics
- PO only
101
thiazide example
hydrochlorothiazide (HCTZ)
102
antiocaogulants action
inhibits the clotting of blood by blocking coagulation pathway, binding with substance or blocing an action
103
anticoagulant uses
prevents clot formation
104
S/E of anticoagulants
- uncontrolled bleeding; no clotting when needed (hemorrhage)
105
3 anticoagulant meds
1. heparin (SQ or IV; antidote = protamine sulfate)
2. lovenox (low mol. weight heparin; lasts longer, easier to absorb)
3. warfarin sodium (coumadin) (PO, IM; antidote is Vit K)
106
antilipidemics
HMG-CoA-Reductase inhibitors = statins
107
statin action
- decreases blood chol. by decreasing rate of chol prod by the liver (blocks an enzyme)
- fewer LDLs, more HDLs
108
statin side effects
few other than body aches
109
statin example
atorvastatin (lipitor)
