Cardiovascular Meds Flashcards
(83 cards)
1
Q
List drug strategies to improve cardiac function
A
- Directly increase cardiac contractility
- Reduce workload of the heart by:
- reducing contractility → direct effect
- reducing afterload → indirect effect
- reducing preload → indiriect
- Increase myocardial blood flow
- Manage hemostasis
- Other
- antiarrhythmic drugs
- statins
2
Q
what are ionotropic agents?
A
used to increase force of contraction
3
Q
T/F: intravenous positive iontrophic agents can be used anywhere
A
FALSE
should only be used in inpatient settings
and then only in pts manifesting S/S of low CO-syndrome
4
Q
T/F: pt services are probably on hold with pts recieving IV ionotropic therapy
A
TRUE
5
Q
List several ionotrophic agents
A
- Dopamine
- Dobutamine
- Milrinone
6
Q
what is the effect of low-dose dopamine?
A
associated with dilation within renal and splanchnic vasculature resulting in enhanced diuresis
7
Q
what is the effect of moderate-dose dopamine?
A
enhances cardiac contractility and HR
8
Q
what is the effect of high-dose dopamine?
A
increased afterload through peripheral vasoconstriction
9
Q
describe dobutamine
A
- +ionotrophic and chronotrophic agent
- (increased contracility and HR)
- decreases afterlod
- beta-receptor agonist
- improved end organ perfusion
- improves MAP
10
Q
describe Milrinone
A
- type 3 phosphodiesterase inhibitor
- increases iontrophy, chronotrophy, and lusitrophy
- contractility, HR, rate of myocardial relaxation
- increases intramyocardial ATP
- potent vasodilator
- used in management of pulmonary HTN
11
Q
what is Digitalis used to treat and how does it work?
A
- Used to treat impaired cardiac contractility typically caused by HF
- works by directly increasing cardiac contracility
- direct ionotrophic effects
12
Q
what else is digitalis referred to as?
A
- Foxglove
- cardiac glycoside
- digoxin
- digitoxin
13
Q
how does Digitalis increase cardiac contracility?
A
- increases Ca2+ influx into myocytes
14
Q
what are the electrophysiological effects of digitalis?
A
- increases the AV node’s refractory period, decreasing the ventricular response (anti-arrhythmic)
- used to treat A-Fib, Atrial tachycardia and HF
- can cause reflex stimulation of the vagus nerve
- decrease HR and contractility
15
Q
List drug classes that work to directly reduce contractility and thus reduce workload of the heart
A
- Beta-blockers
- Ca2+ channel blockers
16
Q
what is the effect on the heart when a beta-1 agonist is given?
A
increased HR
increased contractility
17
Q
what is the clinical use of beta-1 agonists? What is the impact on cardiac work?
A
- Clinical use
- treat conditions of severe cardiac decompensation
- cardiovascular shock
- in conjunction with cardiac surgery
- HF
- treat conditions of severe cardiac decompensation
- Impact on cardiac work
- increases work load of the heart
18
Q
what is the effect on the heart when a beta-1 antagonist is given?
A
decreased HR
decreased contractility
limit impact on sympathetic NS on the heart
19
Q
what is the clinical use of a beta-1 antagonist and what is the effect on cardiac work?
A
- Clinical use
- used to treat compromised or diseased hearts
- Impact on cardiac work
- reduces workload of the heart
- reduces functional capacity
20
Q
T/F: Beta-1 antagonists affect primarily the heart
A
TRUE
(called beta-blockers)
21
Q
what is the effect of beta-blockers on the heart?
A
negative chronotropic and ionotrophic effect
(reduces workload of the heart)
22
Q
differentiate between the 2 subtypes of beta-blockers
A
- non-specific beta-blocker
- positive effect on the heart
- negative effect (smooth muscle contraction) on bronchial smooth muscle
- cardioselective beta-blocker
- specific for B-1 receptors which are found most frequently on cardiac tissue
23
Q
Beta-blockers suffic
A
-olol
24
Q
Adverse effects of beta-blockers
A
- receptor overreach
- can cause bronchoconstriction which is not a problem in most ppl but becomes a problem in those with pulmonary disease (cor pulmonale)
- can cause excessive depression of cardiac function
- OH
- depression, lethargy and sleep disorders (long term use)
- reduced peak HR
- reduced exercise capacity
7.
25
how to calculate HRmax for someone on a beta-blocker
HRmax = 164 - 0.7\*age
26
what is the effect of Ca channel blockers on the heart?
1. reduce calcium entrance into myoctyes causing:
* reduced contractility
* reduced energy demands on heart
* reduced CO
27
AE of Ca channel blockers
1. decreased BP
2. flushing
3. bradycardia
4. HA
5. dizziness
6. peripheral edema
7. May increase risk of MI
\*result in peripheral vasodilation which explains many AE
28
List drugs that reduce afterload
1. Alpha blockers
2. direct vasodilators
3. beta-blockers
4. centrally acting agents
29
what is the effect of alpha blockers?
smooth muscle relaxation, vasodilation and decreased TPR
30
what is TPR?
Total Peripheral Resistance (aka systemic vascular resistance or SVA)
* the resistance to blood flow offered by all of the systemic vasculature beds to blood flow
* largely determined by changes in blood vessel diameter
*
31
AE of alpha blockers
1. these are systemic drugs with systemic effects
2. reflex tachycardia secondary to hypotension
3. OH
4. edema of LE
5. syncope
6. SOB
7. Weakness
8. N/V
32
how do direct vasodilators work?
work directly on smooth muscle cells to cause relaxation and thus reduce afterload and the workload on the heart
33
how can beta-blockers reduce afterload?
reduce vascular smooth muscle contraction and SVR
34
how do centrally acting agents act to reduce afterload?
1. appear to inhibit sympathetic outflow from the brainstem
* decrease HR
* decrease contractility
* decrease TPR
2. act like alpha 2 antagonists
3. often given with a diuretic
35
AE of centrally acting agents
1. dry mouth
2. dizziness
3. drowsiness
4. hypotension
36
how does influencing preload reduce the workload of the heart?
changes in blood volume affect arterial pressure by changing CO
they influence the Frank-Sterling law to reduce LVEDV and thus reduce cardiac contracility
37
list drug classes that work to reduce preload
(and thus reduce the workload of the heart)
1. Diuretics
* loop diuretics
* thiazide diuretics
* potassium sparing diuretics
2. ACE inhibitors
3. ARBs
4. Aldosterone antagonists
38
how do diuretics reduce preload?
they increase the amount of urine formed
* increases diuresis which decreases blood volume
* act directly on the kidneys to increase water and sodium excretion
39
how do loop diuretics work?
1. act on the ascending limb of the loop of Henle
2. inhibit the reabsorption of Na+ and Cl-
3. loss of K+
40
how do thiazide diuretics work?
1. act on the distal convoluted tubules to inhibit Na+ reabsorption
41
how do K+ sparing diuretics work?
1. interfere with sodium-potassium exchange mechanism in distal convoluted tubules
2. are less effective at producing diuresis but are K+ sparing
42
rank the diuretic classes based on AEs
loop \> thiazides \> potassium sparing
43
loop diuretics are used more for \_\_\_\_\_\_\_
diuresis than HTN control
44
Diuretics AEs
1. geriatric pts → more susceptible to resulting hypotension
2. dehydration
* OH
* increased TPR
* activate renin-angiotensin system
3. Electrolyte imbalance
* hyponatremia → AMS
* hypernatremia → cardiac dysrhythmias
4. OH and falls precaution
5. Can cause urinary incontience secondary to increased urine production
45
why do pts on diuretics call them "water pills?
they will frequently require bathroom breaks and
46
S/S of toxicity from diuretics
1. anorexia
2. N/V
3. confusion
4. increased weakness
5. paresthesia
47
List all the effects angiotension II has
1. constricts walls of arterioles
2. stimulates Na+ reabsorption in the kidneys
3. stimulates aldosterone release from adrenal cortex which causes kidneys to reclaim still more sodium and water
4. stimulates catecholamine release
5. net effects
* vasoconstriction
* fluid retention
* increased afterload
48
what is the entire goal of the renin-angiotensin system?
preserve water and electrolytes
49
what are the net effect of ACE Inhibition?
1. decreased vascular smooth muscle tone
2. inhibition of aldosterone secretion
3. decreased renin activity/production
50
AE of ACE inhibitors
typically well tolerated
1. allergic reaction (some may have this and it presents like a cough)
2. GI discomfort
3. Dizziness
4. Chest pain
5. Persistent cough
6. Weakness
51
suffix for ARBs
(ARBS = angiotensin II receptor antagonists)
suffix = -artan
52
what is aldosterone?
a steroid hormone produced by adrenal cortex
* plays a central role in regulating BP
* acts at the level of the distal convoluted tubule and collecting ducts
* increases reabsorption of ions (Na+) and water in the kidney
* conserves Na+, secretes K+, increases water retention, increases BP
53
list classes of drugs available to treat HTN
1. Direct vasodilators
2. Beta-adrenergic blockers
3. Centrally acting agents
4. Alpha blockers
5. Ca+ channel blockers
6. ACE Inhibitors
7. Angiotensin II receptor antagonists (ARBs)
8. Diuretics
9. Aldosterone receptor blockers
54
list drug classes that work to increase blood flow to the myocardium
(thus increasing myocardial blood flow)
1. Nitrates
* organic nitrates
* nitroglycerin patches
55
how do nitrates work on the myocardium?
1. venodilator → decrease venous return and decrease preload
2. arteriodilator → decrease afterload
3. acts as a relaxant for coronary artery smooth muscle and systemic arterial smooth muscle
56
T/F: organic nitrates like nitroglycerin act specifcally on coronary arteries
FALSE
they produce a general vadodilation not specifically a coronary artery dilation
57
how can nitroglycerin be delivered?
1. Oral → first pass effect is substantial
2. Sublingual → best method to treat acutely/avoids 1st pass effect
3. Buccal → cheek and gum
4. Transdermal patches → prophylactic
58
things to remember with nitroglycerin patches
1. not effective acutely/immediately
2. must be changed every 24 hrs
3. change where patch is applied to avoid skin rash
4. always use it even if you are feeling well
5. don't suddenly stop using it
6. don't double up if patch is forgotten
7. dispose of used
59
when should a pt contact an MD when they are on a nitroglycerin patch?
if they develop blurred vision, dry mouth, skin rash, dizziness, or fainting
60
List drugs that manage hemostasis
1. Thrombolytic agents
2. Antiplatelet agents
3. Anticoagulants
61
what is hemostasis?
1. Intrinsic process which causes bleeding to be stopped
2. requires the combined activity of vascular, platelet and plasma factors
* vessel wall injury trigger attachment and activation of platelets and causes vasoconstriction
* platelets become "sticky" and attach to the area of vessel wall injury
* plasma factors interact to convert fibrinogen to fibrin which helps form clot
62
how do thrombolytics work?
act by degrading a **formed** clot
63
AE of thrombolytics
1. hemorrhage
2. be alert for signs of heavy bleeding
* severe HA
* joint or back pain
3. no antidote
4. GI distress
5. unusal bleeding
64
unusal bleeding sites that may occur when a pt is on thrombolytics
1. nose bleeds
2. blood in urine or stool
3. bruising
4. unusually heavy menstrual flow
5. back pain or joint pain may indicate abdominal or joint hemorrhage respectively
65
what are anticoagulants?
chemical substances that help prevent or slow the coagulation of blood (formation of clots)
* these are preventative
* commonly called blood thinners
* act by interfering with the proteins in the blood that are involved in the coagulation process
66
list some drugs that are anticoagulants
1. Heparin
2. Coumadin (Dicoumarol, Warfarin)
3. Xarelto
4. Eliquis
5. Lovenox
67
Anticoagulants are used primarily to treat \_\_\_\_\_
1. strokes
2. MIs
3. DVT
4. PE
5. Hx of blood clots, post surgery, inactivity
6. A-Fib
68
AE of anticoagulants
1. Hemorrhage
2. bruising, bloody stools, bleeding gums, blood in urine, ecchyomosis
3. thrombocytopenia
4. back pain, joint pain
* bleeding into the abdomen or a joint
5. GI distress
69
Special Concerns for rehab pts on anticoagulants
1. know why your pt is on an anticoagulant
2. while using this med, it is very important that one avoids contact sports and other activities that may cause you to be injured
3. do not use with aspirin concurrently
4. take special care in brushing teeth and in shaving
* soft toothbrush and floss gently
* best to use electric shaver over a blade
70
how do antiplatelet drugs work?
prevent platelets from clumping together to form a clot
* aspirin is a classic drug in this class
* may also be called blood thinners
71
what is an arrhytmia?
any significant deviation from normal cardiac rhythm
can result in:
1. impaired pump function
2. cardiac failure
3. CVAs
4. death
72
List several mechanisms for a cardiac arrhytmia
1. abnormal pulse generation
* defects in SA or AV nodes
* ectopic foci
2. abnormal pulse conduction
* abnormality in conduction pathway
* AV block
* Bundle branch block
3. a combo of these
73
Drugs that treat arrhythmias
1. Class I drugs → Na+ channel blockers
2. Class II drugs → Beta blockers
3. Class III drugs → prolong myocyte repolarization
4. Class IV → Ca+ channel blockers
74
describe Class I anti-arrhythmic drugs
Na+ channel blockers
1. normalize the rate of Na+ influx into the cell
2. stabilize the membrane and reduce membrane excitability
3. lidocaine is an example
75
describe Class II anti-arrhythmic drugs
Beta Blockers
1. main stay of arrhythmia trx
2. diminish the influence of the excitatory effects of the sympathetic NS
3. decreases cardiac automaticity
4. lengthens the effective refractory period resulting in a slower HR
76
T/F: being on a beta-blocker reduces the liklihood of a second MI
TRUE
77
describe Class III anti-arrhythmic drugs
Prolong myoctye repolarization
1. inhibit K+ efflux
2. slows/stabilizes HR
3. used to treat ventricular arrhythmias
78
describe Class IV anti-arrhytmic drugs
Ca+ Channel Blockers
1. normalize Ca++ entry into the channel thus controlling excitability and the conduction of cardiac tissue
2. Verapamil, diltiazem
79
T/F: not all Ca++ channel blockers are effective in managing cardiac arrhythmias
TRUE
80
Statins are _________ lowering drugs
cholesterol
81
what drugs are used to treat hyperlipidemia?
HMG-CoA Reductase Inhibitors (Statins)
82
how do statins help treat hyperlipedmia?
1. decreased cholesterol synthesis
2. increased removal of LDLs from blood
3. some can increase HDLs
4. stabilize athersclerotic plaques
5. reduce risk for an MI
83
AE of Statins
1. Rhabdomyolysis
2. Muscle pain
3. liver damage → pt should have quarterly liver panels
4. drug intolerance
5. HA
6. abdominal pain
7. constipation
8. Loss of Co Enzyme Q10
