1
Q
drug strategies to improve cardiac function
A
- directly increase cardiac contractility
- reduce work load of the heart
- increase myocardial blood flow
2
Q
How do drugs reduce workload of the heart
A
- reduce contractility (direct)
- reduce afterload (indirect)
- reduce preload (indirect)
3
Q
Cholinergic receptors
A
- muscarinic
- nicotinic
activated by ACH
4
Q
Andrenergic Receptors
A
- alpha (1 and 2)
- beta (1 and 2)
activated by NE
5
Q
Beta-1 agonists:
response when stimulated
A
increased HR and contractility
6
Q
Beta-1 agonists:
clinical use
A
treat conditions of cardiac decompensation
7
Q
Beta-1 agonists:
impact
A
increases work load of the heart
8
Q
Beta-1 antagonists:
response when stimulated
A
- decreased HR and contractility
2. limit impact of sympathetic NS on heart
9
Q
Beta-1 antagonists:
clinical use
A
treat compromised or diseased hearts
10
Q
Beta-1 antagonists:
impact
A
- reduce work load of the heart
2. reduces functional capacity
11
Q
What are some conditions of cardiac decomposition (low CO)
A
- CV shock
- HF
12
Q
Ionotropic agents used to:
A
- increase force of contraction
13
Q
When should IV + ionotropic agents be used
A
- inpatient settings
- volume overload with evidence of organ hypofusion
14
Q
T/F: PT probably on hold with patients receiving IV ionotropic therapy
A
True
15
Q
Ionotropic Agents:
Dopamine
A
naturally occurring catecholamine
precursor to NE
16
Q
Ionotropic Agents:
Dopamine low dose
A
renal and splanchnic vasculature dilation = enhanced diuresis
17
Q
Ionotropic Agents:
Dopamine mod dose
A
enhance cardiac contractility and HR
18
Q
Ionotropic Agents:
Dopamine high dose
A
increased afterload through peripheral vasoconstriction
19
Q
When is dopamine used for cardiac trx?
A
- severe HF
2. moderate HTN
20
Q
Ionotropic Agents:
Dobutamine
A
- beta receptor agonist.
- increases inotropy and chronotropy
- decreases afterload
- improves end organ perfusion (improves MAP)
21
Q
Ionotropic Agents:
Milrinone
A
- 3 phosphodiesterase inhibitor
- increases inotropy, chronotropy, and lusitropy = increased rate of myocardial relaxation
- increases intramyocardial ATP
- potent vasodilator
- management of pulm HTN
22
Q
Digitalis is used to treat
A
- impaired cardiac contractility (HF)
- A-Fib
- tachycardia
- HF
23
Q
T/F: Digitalis increases CO at rest and during exercise but does not prolong life
A
True
24
Q
How does digitalis work
A
- increases CA2 influx into myocytes
2. Increases AV node’s refractory period, decreasing ventricular response
25
Digitalis can cause reflex stimulation of the vagus nerve, resulting in:
decreased HR and contractility
26
Drug strategies to improve cardiac function
1. Directly increase cardiac contractility
2. Reduce work load of the heart (reduce contractility and O2 demand)
3. Increase myocardial blood flow
27
drug strategies to reduce work load of the heart
- directly reduce contractility
- reduce afterload
- reduce preload
28
drug strategies to increase myocardial blood flow
- increase blood flow
| - manage hemostasis (manage clots)
29
How do beta blockers work
- antagonists to B-1 receptor
| - have negative chronotropic and ionotropic effects (reduces workload)
30
Non-specific beta blockers
- positive effect on heart.
| - negative effect on bronchial smooth muscle
31
Cardioselective beta blockers
specific for B-1 receptors
32
Beta-1 specific antagonists:
| Adverse Effects
1. receptor over reach: causes bronchoconstriction
2. excessive depression of cardiac function
3. OH
4. depression, lethargy, sleep disorders
5. reduced peak HR
33
How do CCB work?
1. reduce calcium entrance into myocytes
| 2. reduces contractility, energy demands on heart, and CO
34
CCB AE:
1. peripheral vasodilation
2. decreased BP
3. flushing
4. bradycardia
5. headaches
6. dizziness
7. peripheral edema
8. increased risk of MI
35
examples of CCB
1. dilitiazem (cardizem)
2. felodipine (plendil)
3. verapamil
4. nifedipine (procardia)
36
reduced afterload has what effect on O2 consumption
Reduced double product
37
Where are alpha 1 receptors located?
vascular smooth muscle
38
stimulation of a1 receptors causes
smooth muscle contraction = vasoconstriction = decreased radius
39
blockade of a1 receptors (using a1 blockers) results in
smooth muscle relaxation = vasodilation = increased radius = reduced TPR = reduced afterload
40
A1 blockers
| AE:
1. reflex tachycardia secondary to HTN
2. OH
3. Edema of LE
4. Syncope
5. SOB
6. Weakness
7. N/V
41
A1 blocker examples
1. doxazosin
2. prazosin
3. terazosin
42
How do vasodilators work
act directly on smooth muscle relax and increase vascular radius
43
vasodilators:
| hydralazine
1. increases membrane permeability to K
| 2. hyperpolarization of smooth muscle cells
44
vasodilators:
| minoxidil
1. increases membrane permeability to K
| 2. hyperpolarization
45
vasodilators:
| diazoxide
increase membrane permeability to K
46
vasodilators:
| Nitroprusside
causes the release of nitrous oxide
47
beta blocker: effect on kidney
- decrease renin release from kidney
- decreases angiotensin II
- decreased blood volume
48
beta blockers: AE
1. bradycardia
2. dizziness
3. vertigo
4. gastric discomfort
5. sexual dysfunction
6. joint pain
7. bronchospasm
49
estimating HR max on beta blockers
164-(0.7 x age)
50
central acting agents
- inhibit sympathetic outflow from brainstem
- decreased HR, contractility, and TPR
- often given with a diuretic
- act like alpha 2 antagonists
51
central acting agents:
| AEs
1. dry mouth
2. dizziness
3. drowsiness
4. hypotension
52
central acting agent examples
- clonidine
- guanabenz
- guanfacine
- methyldopa
53
Diuretics
- increase the amount of urine formed
- increase diuresis
- decrease blood volume
- acts directly on kidneys to increase water and Na exertion
- inexpensive
54
Loop diuretics
- acts on ascending limb of loop of henle
- inhibits reabsorption of Na and Cl
- Loss of K
- used more for diuresis than HTN
55
Thiazide diuretics
- acts on distal convoluted tubules to inhibit Na reabsorption
56
K sparing diuretics
- interfere with Na-K exchange mechanism in distal convoluted tubules
- less effective at producing diuresis but are K sparing
57
why do geriatrics need to be started on lower doses of diuretics?
they are more susceptible to resulting hypotension
58
Diuretics: AE
1. dehydration
2. hyponatremia=AMS
3. hypokalemia = cardiac dysrhythmias
4. OH
5. urinary incontinence
6. toxicity = anorexia, N/V, confusion, weakness, paresthesia
59
Angiotensin II
- constricts walls of arterioles
- stimulates Na reabsorption in kidneys
- stimulates aldosterone release from adrenal cortex (reabsorb Na and water)
- Stimulates catecholamine release
- vasoconstriction and fluid retention = increased afterload
60
ACE inhibition net effects
1. decreased smooth vascular tone
2. inhibition of aldosterone secretion ( reduced Na and H2O resorption )
3. decreased renin activity/production
61
ACE inhibitors:
| AE
typically well tolerated
1. allergic rxn
2. GI discomfort
3. dizziness
4. chest p!
5. persistent cough
6. weakness
62
where is aldosterone produced?
adrenal cortex
63
where does aldosterone act
distal convoluted tubule and collecting ducts
64
what does aldosterone do?
- increases reabsorption of Na and water in the kidney
| - conserves Na, secretes L, increases water retention and BP
65
Aldosterone antagonists
- act as blocker of aldosterone binding sites
- eplerenone
- spironolactone
66
How do Nitrates work?
- venodilator: dec venous return (preload)
- arteriodilator: dec afterload
- acts as relaxant for CA smooth muscle and systemic arterial smooth muscle
67
T/F: Nitroglycerin produces vasodilation specifically for coronary arteries
False
general dilation
reduces preload and afterload
68
Organic Nitrates for angina pectoris:
| MOA
- dec preload and afterload leads to dec cardiac work and dec O2 use
- dec in MVO2 ( cardiac O2 use) is more important than the increased O2 availability
69
Delivery of Nitroglycerin
Oral: 1st pass effect substantial
Sublingual: Best method acutely to avoid 1st pass effect
Buccal
Transdermal: prophylactic
70
Isosorbide Dinitrate
- treats acute episodes and given to prevent angina onset
| - long acting
71
isosorbide-5-mononitrate
- long acting
| - used primarily for prevention of angina rather than treating an acute situation
72
Nitroglycerin Patches
- not effective acutely
- must be changed every 24 hrs
- change where patch is applied to avoid skin rash
- always use, even if you feel well
- don't suddenly stop
73
T/F: If you forget a patch, don't double up. Just apply 1 as soon as possible
True
74
When should you contact an MD when taking Nitroglycerin patches?
blurred vision, dry mouth, skin rash, dizziness, or fainting
75
Hemostasis
- process which causes bleeding to be stopped
| - requires the combined activity of vascular, platelet, and plasma factors
76
Hemostasis:
| vessel wall injury
triggers attachment and activation of platelets and causes vasoconstriction
77
Hemostasis:
| Platelets
become sticky and attach to area of injury
78
Hemostasis:
| Plasma factors
interact to convert fibrinogen to fibrin which helps form clot
79
Thrombogenesis
- formation of clot (thrombus)
- can lead to localized vessel occlusion
- may dislodge and form embolism
80
Embolism
blood clot that has moved from site in bloodstream to another site. obstruct artery and block flow
81
Fibrinolysis
process that involves break down or degradation of thrombus
82
Anticoagulants
- act by controlling function/synthesis of clotting factors
Heparin
Coumadin
83
Antithrombotics
Act by inhibiting platelet function (prevents thrombus formation)
- aspirin
- plavix
84
T/F: Oral anticoagulants require several days to achieve therapeutic levels
True
| may be taken for weeks - months
85
Warfarin
- inhibits vit k action
| - antidote: treat with vit k and d/c
86
Pradexa
- acts as direct thrombin (factor IIa) inhibitor
| - reduce risk of CVA and thrombosis in patients with nonvalvular afib
87
anticoagulants:
| AE
1. excessive bleeding
2. bruising
3. bloody stools and urine
4. bleeding gums
5. ecchyomosis
6. thrombocytopenia
7. back and joint pain due to bleeding into abdomen or joint
8. GI distress
88
anticoagulants:
| special concerns for rehab
1. know why your pt is on an anticoagulant
2. avoid contact sports and risky activities
3. don't use w/aspirin
4. take care brushing teeth and shaving
89
antithrombotics:
| Aspirin
1. suppresses synthesis of prostaglandins and thromboxanes via COX 1 and 2 enzymes
2. prophylactic trx for preventing MIs
90
antithrombotics:
| dipryridamole
reduces adenosine metabolism and/or cAMP levels in platelets
91
antithrombotics:
| clopidgrogel (plavix)
inhibit ADP binding to platelets
92
antithrombotics:
| AE
1. hemorrhage
2. severe HA
3. joint/back p!
4. GI distress
no antidote
93
when are thrombolytic drugs used
- facilitate breakdown and dissolution of clots that have already formed
- facilitate formation of fibrinolysin
- MIs, CVAs, PEs, acute peripheral arterial occlusion, occlusion of indwelling catheters
94
thrombolytics:
| AE
#1. hemorrhage
- nose bleeds
- blood in urine/stools
- bruising
- unusually heavy menstrual flow
- back p! or joint p!
95
arrhythmias can result in
1. impaired pump function
2. cardiac failure
3. CVAs
4. death
96
mechanisms of cardiac arrhythmias
1. abnormal pulse generation
2. abnormal pulse conduction
3. combo of these 2
97
Arrythmias:
| abnormal pulse generation
- defects in SA or AV nodes
| - ectopic foci
98
Arrythmias:
| abnormal pulse conduction
- abnormality in conduction pathway
| - AV block, bundle branch block
99
Management of Arrhythmias:
| Class I Drugs
1. Na channel blockers
- normalize rate of Na influx into cell
- stabilize membrane and reduce membrane excitability
2. Lidocaine- helps manage EKG abnormality / defects during early portion of AP
100
Management of Arrhythmias:
| Class II Drugs
Beta Blockers
- primary arrhythmia trx
- diminish influence of excitatory effects of sympathetic NS
- dec cardiac automaticity
- lengthens effective refractory period (slower HR)
101
Management of Arrhythmias:
| Class III Drugs
Prolong myocyte repolarization:
- inhibit K efflux
- slows/stabilizes HR
- used for ventricular arrythmias
102
Management of Arrhythmias:
| Class IV Drugs
CCBs
- normalize Ca entry into channel which controls excitability and conduction of tissue
not all CCB are effective in managing arrythmias
103
HMG-CoA Reductase Inhibitors / Statins
- enzyme catalyzes rate of limiting step in cholesterol biosynthesis
- dec cholesterol synthesis
- inc removal of LDLs from blood.
- inc synthesis of HDLs
- stabilize atherosclerotic plaque
- reduce risk for MI
104
HMG-CoA Reductase Inhibitors / Statins
| AEs
1. rhabdomyolysis
2. tell pts to promptly report muscle p!, tenderness, or weakness
3. liver damage
4. drug intolerance
5. HA
6. abdominal p! and constipation
7. loss of coenzyme Q10
105
Rhabdomyolysis
destruction of skeletal muscle
Cardiopulm
flashcards
Decks in class (20)
# Cards
-
cardiac anatomy61
-
cardiac physiology54
-
Cardiac Physiology - Heart29
-
Rakotz BP11
-
Heart Failure33
-
Ischemic Heart Disease25
-
HTN heart disease26
-
cardiomyopathies26
-
Other cardiac pathologies32
-
CV meds105
-
Diagnostic cardiac blood tests81
-
Other cardiac dx tests23
-
cardiac interventions86
-
cardiac evaluation59
-
Exercise 10132
-
Exercise Testing28
-
Exercise Prescription30
-
Cardiac Rehab26
-
respiratory system58
-
Pulmonary Evaluation39
