CV block 5 Flashcards
Cardiovascular Block 5
1
Q
what are cardiac stimulants?
A
stimulate heart function. stronger, faster
2
Q
Cardiac Stimulants drugs
A
Adrenergic Agonists, Cardiac Glycosides
3
Q
Antihypertensives – reduce blood pressure
A
Adrenergic Blockers, Calcium Channel Blockers, ACE/angiotensin II inhibitors, diuretics, vasodilators, alpha2 agonists, nitrates
4
Q
how does antihypertensive drugs work?
A
reduces workload of the heart
5
Q
Drugs to reduce vascular occlusions
A
anticoagulants, antiplatelets, thrombolytics.
Improve blood supply
6
Q
Drugs to reduce atherosclerotic potential
A
lipid lowering drugs
-reducing plasma cholesterol and triglyceride levels
7
Q
what is Inotropic effect?
A
where there is a change in the contractile force in the heart
8
Q
what is chronotropic effect?
A
where there is a change in the heart rate.
- slow beat
+ fast beat
9
Q
what is dromotropic effect?
A
where there is a change in the conduction speed of electrical impulses in the heart
10
Q
examples of sympathomimetics drugs?
A
adrenaline, dopamine, dobutamine
11
Q
what is the clinical use of adrenaline/epinephrine?
A
used in circulatory shock, hypotension and cardiac arrest
12
Q
how does adrenaline acts?
A
acts on B1-receptors in heart for + inotropic and chronotropic effect
13
Q
How’s adrenaline administered?
A
IV or IM
14
Q
Adrenaline adverse effect?
A
nausea, hypertension, constipation, tachycardia
15
Q
what does dopamine do to the body?
A
produces positive inotropic effects on the heart, reducing its workload and maintains renal blood flow.
16
Q
how dopamine administered?
A
IV
17
Q
common adverse effect of dopamine
A
increase HR, vasoconstriction, hypotension tolerance, nausea/vomiting
18
Q
Dobutamine
A
Has positive inotropic effect by stimulating the b1-receptors
19
Q
how does dobutamine works?
A
Less vasoconstriction in the peripheries so if an IV line - less likely to cause tissue damage
20
Q
onset and life of dobutamine
A
action in 5 minutes and short half life.
21
Q
use of digoxin
A
is no longer the first choice for congestive heart failure, but can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment.
22
Q
effectivity and ineffectively of digoxin
A
- ineffective at decreasing long term morbidity and mortality in Congestive Heart Failure.
- increase quality of life in short/medium term.
23
Q
Digoxin clinical application
A
CHF and atrial fibrillation
24
Q
How is digoxin eliminated from the body?
A
via kidney
25
what is the half life of digoxin?
40 hours
5 x 40 hrs – 6 x 40 hrs
= 200 hrs – 240 hrs
= 8.3 -10 days
26
therapeutic index of digoxin?
narrow therapeutic index drug
27
adverse effects of digoxin?
Loss of appetite, nausea and vomiting, and abdominal
| distress may indicate digoxin toxicity.
28
GI disturbances of digoxin?
s (anorexia; diarrhoea); nausea and vomiting
29
CNS effects of digoxin?
disorientation, visual disturbances, confusion, hallucinations
30
digoxin interaction with potassium
- high K+ levels= decreased digoxin activity
| - low K+ levels = increased digoxin activity
31
drug interaction of digoxin
- cause hypokalaemia=Loop diuretics, Corticosteroids, Lithium,
- Calcium channel blockers, ACE inhibitors, antacids..
32
digoxin care
- monitor K levels
- monitor toxicity
- check renal function
- HR, need to be 60+
- monitor serum digoxin levels
33
what is the antidote for digoxin?
digibind IV
34
Which is NOT a sympathomimetic
| agonist?
acetylcholine
35
Digoxin has which of the following effects on the
| heart?
positive inotropic and negative chronotropic
36
peripheral vasodilators clinical applications
angina, CHF, hypertension
37
use of peripheral vasodilators
to reduce workload on the heart.
38
Peripheral Vasodilators acts on veins: nitrates
reduce preload; so decrease cardiac
| output and tissue perfusion
39
peripheral vasodilators act on arterioles: hydralazine, nitroprusside
reduce cardiac afterload; so decrease cardiac workload and increase cardiac
output and tissue perfusion
40
nitrate mode of action
1. Nitrates are converted into nitric oxide (NO).
2. NO increases the intracellular levels of cGMP
3. cGMP causes decrease in calcium ions within
the muscle cells.
41
result of nitrate MOA
the blood vessels (veins) dilate, relax. This venodilation means that preload is reduced.
42
nitrates adverse effects
– headache, facial flushing,
| hypotension, rebound tachycardia
43
use of morphine
```
a venodilator (useful in pulmonary oedema due to reducing pulmonary hypertension)
-decreases BP, therefore workload on the heart
```
44
Glyceryl trinitrate (GTN) is a critical component of:
dynamite
45
Nitrate vasodilators act mainly on:
veins
46
For patients with diabetes or chronic renal disease this is
| lower:
130/80 mmHg
47
normal BP
below 140/90 mmHg
48
For patients with heart failure (or post MI) a lower blood pressure is desirable
110/70
49
Drugs Used to Treat Hypertension
-A is for ACE inhibitors,
ARBs (Angiotensin II-Receptor Blockers), alpha antagonists, alpha2 agonists
-B is for b-blockers
-C is for CCBs (calcium channel blockers) & Combined action drugs
-D is for Diuretics
50
Alpha Blockers drugs
terazosin & doxazosin
51
Mode of Action Alpha Blockers
block the a1-receptor sites and reduces sympathetic nervous system response. stops neurotransmitters binding.
52
Adverse effects of alpha blockers
postural hypotension, nasal congestion, fatigue, inhibition of ejaculation, lack of energy
53
Clinical Application of alpha blockers
control of hypertension, peripheral vascular disease, urinary retention.
54
how is alpha blockers administered?
orally
55
Beta-Blockers has 4 useful actions in hypertension.
- Block beta receptors in the heart- decrease heart rate and contractility therefore decreases cardiac output and BP
- Suppress reflex tachycardia caused by vasodilator
- Reduce the release of renin by the kidneys, hence less fluid retention
- Long term use reduces peripheral vascular resistance
56
Beta-Blockers drugs
metoprolol, atenolol, carvedilol
57
Beta-Blockers clinical applications
cardiac disease, hypertension, angina, migraine prophylaxis
58
Beta-Blockers mode of action
: block β-1 receptors in the heart muscle therefore decreases cardiac output and BPdecreases.
59
Beta-Blockers administration
orally
60
Non-selective drugs
labetalol
61
Non-selective drugs blocks
* Blocks a1 and b-receptors.
| * Can be used for pregnancy induced hypertension
62
how are Non-selective drugs administered
orally or IV
63
Selective b-blockers drugs
target b1-receptors which
predominate in the heart eg. atenolol (Tenormin),
metoprolol (Lopressor)
64
What are the inotropic and
| chronotropic effects of beta blockers?
negative
65
Do not discontinue β-blocker therapy quickly as it
| could cause?
rebound hypertension, angina, dysrhythmia and MI.
66
Contraindication of Beta-Blockers
-COPD, asthma
-Bradycardia (45-50 bpm)
-Cardiogenic or hypovolaemic shock
-Severe hypotension
-Should be avoided in diabetes (especially
nonselective adrenergic blockers)
67
a2-Agonists drugs
methyldopa, clonidine
68
adverse effects of a2-agonists drugs
fatigue, hypotension,
inhibition of ejaculation,
nasal congestion
69
Calcium Channel Blockers (CCBs) drugs
amlodipine, felodipine, diltiazem
70
Calcium Channel Blockers (CCBs) clinical applications.
angina, hypertension
71
Calcium Channel Blockers (CCBs) MOA.
blocks calcium channel and
stops calcium entering into the vascular and
cardiac cells.
72
What are the inotropic and chronotropic effects of
| calcium channel blockers?
Negative!!
73
Adverse effects - CCBs
decreased BP, headache, abdo discomfort, peripheral edema, decreased HR
74
CCBs - Drug Interactions
• β-blockers
• Digoxin
• Inhibitors of CYP3A4
(e.g. erythromycin, grapefruit juice)
75
what is Nimodipine
selective for cerebral blood vessels
76
how Nimodipine affects the brain?
will increase cerebral blood flow particularly to damaged areas of the brain.
77
antidote for Overdosing nimodipine
Treat with activated charcoal and whole bowel irrigation
78
ACE inhibitors drugs
captopril, enalapril
79
Angiotensin II antagonists (ARBs) drugs
losartan
80
diuretics drugs
aprinox, frusemide (lasix), spironolactone
81
Angiotensin Converting EnzymeInhibitors (ACE Inhibitors) drugs and clinical application
- cilazapril, quinapril (prodrugs)
| - hypertension
82
how ACE inhibitors administered?
orally.• Usually given in combination with diuretics
83
What is a prodrug?
-administered in an inactive (or significantly less active) form. once administered, the prodrug is metabolised
into an active metabolite
84
Adverse Effects - ACE Inhibitors
hypotension, unproductive cough, taste disturbances, headache, GI upset, hyperkalaemia
85
ACE inhibitors Drug Interactions
diuretics, lithium, NSAIDs
86
Angiotensin Receptor Blockers (ARBs) drugs (ends with sartans)
losartan, candesartan
87
Angiotensin Receptor Blockers (ARBs) clinical application
hypertension, heart failure.
88
Angiotensin Receptor Blockers (ARBs) can be combined with?
diuretics
89
What are the
| adverse effects ARBs?
ARBs block AT1 receptors
-headache, hypotension,
dizziness, GI disturbances
90
Angiotensin Receptor Blockers (ARBs)
* Generally well tolerated
* NO unproductive cough
* reduced risk of hyperkalaemia
* maximum effect seen 4-6 weeks
91
what does diuretics do?
- reduce circulating fluid
- reduce blood pressure and oedema by increasing urine production.
- All diuretics enhance water and sodium excretion
92
Thiazides drugs
bendroflumethiazide, hydrochlorothiazide
93
Clinical Application of thiazides?
drug of choice for management of
| hypertension [mild to moderate].
94
mode of action of thiazides
act on distal convoluted tubule of nephron and decreases sodium reabsorption, increases
concentration of fluid entering collecting ducts and induces diuresis
95
adverse effects of thiazides
dehydration, hyponatraemia,
| hypokalaemia, hyperglycaemia
96
Loop Diuretics drugs
frusemide (lasix)
97
clinical application of loop diuretics
states of oedema: CHF
98
mode of action of loop diuretics
nhibit reabsorption of sodium and
| chloride ions from Loop of Henle into interstitial fluid.
99
adverse effects of loop diuretics
: dehydration, hyponatraemia, hypokalaemia, dizziness, headaches, deafness
100
loop diuretics drug interactions?
increase digoxin and lithium toxicity
101
Potassium Sparing Diuretics types include
- Spironolactone
| - Amiloride
102
Spironolactone [aldosterone antagonist]
Inhibits the action of aldosterone in the distal tubule leading to sodium loss and potassium being retained.
103
Amiloride
acts directly on K+/Na+ interchange in the distal tubule causing Na+ loss and K+ retention
104
Potassium Sparing Diuretics clinical application
used mainly in the prevention of potassium loss from the use of other diuretics.
105
Osmotic Diuretics drugs
Mannitol ------ Administered by IV only
106
Clinical application of Osmotic Diuretics
states of oedematous (e.g.
glaucoma, elevation of intracranial pressure); CHF;
emergency situations.
107
Mode of Action of Osmotic Diuretics
expand extracellular fluid and plasma volume which increases blood flow to kidney, increases osmolarity of blood and renal filtrate and promotes diuresis.
108
Adverse effects of Osmotic Diuretics
electrolyte imbalance, dehydration,
| hypovolaemia
109
Characteristics of Mannitol:
- Relatively non-toxic
- Excreted quickly
- Is not reabsorbed from glomerular filtrate
- Water soluble or hydrophili
110
Antihypertensives- An annoying adverse effect of ACE inhibitors is:
a dry, unproductive cough
111
Examples of Angiotensin receptor blockers are:
Losartan & candesartan
112
An example of an osmotic diuretic is:
mannitol
113
Anticoagulants drugs
Heparin, Warfarin, Dabigatran
114
Antiplatelet drugs
Aspirin
115
Thrombolytics drugs
Streptokinase, Urokinase, TPA*
116
what is heparin?
occurs naturally in the body and is found i mast cells. acts by augmenting the function Antithrombin III, a natural inhibitor of coagulation
117
how is heparin administered?
IV fast action or SUBCUT slower action.
118
adverse effect of heparin
haemorrhage. others include hypersensitivity and thrombocytopenia
- safe in pregnancy
119
what to do when there's too much heparin
discontinue treatment when haemorrhaging occur. administer Protamine Sulphate slowly-severe bleeding
120
other heparin drugs- low molecular weight heparin (fragmin)
longer half-life, can be used by outpatients post-MI, easily be self administered
121
what is warfarin?
long term anticoagulant therapy. it inhibits epoxide reductase which oxidises Vit K for reuse
122
warfarin compared to heparin
slower onset of action 12-24
longer duration of action 3-5
narrow therapeutic index
123
food high in Vit K
cabbage, cauliflower, broccoli, brussel sprouts, spinach, parsley, onions, liver
124
antiplatelets -aspirin
platelets bind to damaged endothelial walls, blocked by aspirin, thromboxane produced= vasoconstrictor, further platelet aggregation, promotes clot formation
