4. CARDIOVASCULAR SYSTEM Flashcards
1
Q
…form physiological system that is responsible for supply of O2 and nutrients to organism and participation in elimination of metabolic waste
A
-heart, blood, blood vessels and lungs
2
Q
effectiveness of cardiac muscle depends upon
A
O2 levels in blood
3
Q
function of heart is regulated by
A
autonomous nervous system that controls its rhythm and contractility
4
Q
heart is impacted by
A
-catecholamines (noradrenaline)
-dopamine
-prostaglandins
-acetylcholine
-renin-angiotensin-aldosterone system
5
Q
cardiac muscle contraction mechanism: following stages (7)
A
- increase in myofibril membrane permeability for Na ions > flow of Na ions across membrane into cell and depolarization of membrane
- entry of Ca ions into cells and/or release from sarcoplasmic reticulum
- increase in concentration of Ca in cell will lead to reaction between ATP, myosin and actin > result ATP release > myosin-actin complex is formed and contraction occurs
- expulsion of K from cell with participation of Na, K-ATPase and depolarization of membrane terminated access of Ca into cell
- potential of cell membrane depends upon difference in concentrations of Na and K ions inside cell and external surface of cell
- cell membrane is selectively more permeable for K ions during diastole compared to Na
- this results in different charges occurring between internal and external surface and action of sodium-potassium pump becomes possible
6
Q
positive inotropic effect
A
-systolic contraction of heart becomes faster and improves
-tone of myocardium improves
-dimension of dilated myocardium are reduced > minute and beat rate increase
-blood circulation becomes faster
-venous blood pressure drops=lisäävät sydänlihaksen supistumisvoimaa
7
Q
negative chronotropic effect
A
slow-down in heart beat=hidastaa sydämen sykettä
8
Q
negative dromotropic effect
A
inhibitor of impulse formation and impulse transmission system =Ne hidastavat impulssien johtumista sydämen johtoradassa.
9
Q
positive bathmotropic effect
A
increase in myocardial irritability
10
Q
substances impacting cardiac function: cardiotonics
A
-substances that restore energy resources of heart
-primarily for treatment of chronic heart failure
11
Q
substances impacting cardiac function: cardiac stimulants
A
-substances that mobilize on short-term basis energy resources of heart
-used temporarily stimulate heart
12
Q
ACE inhibitors
A
Angiotensin-converting-enzyme inhibitors
13
Q
ACE inhibitors: mechanism of action
A
-inhibit conversion of inactive angiotensin 1 to active angiotensin 2 > reduces arteriolar resistance and glomerular filtration rate in glomerular capillaries
14
Q
angiotensin is polypeptide that
A
-constricts blood vessels
-increases secretion of aldosterone
-facilitates central and peripheral effects of sympathetic nervous system
15
Q
ACE inhibitors increase concentration of
A
bradykinin
16
Q
activity of noradrenaline is reduced and activity is increased in
A
plasma
17
Q
vasoconstrictor effect of angiotensin 2 is
A
reduced
18
Q
excretion of sodium and water is
A
increased
(angiotensin 2-mediated release of aldosterone is decreased: aldosterone-mineralocorticoid, responsible for reabsorbtion of water and ions in kidney)
19
Q
vasodilator effect of
A
bradykinin is maintained
20
Q
REPRESENTATIVES of ACE inhibitors
A
-benazePRIL
-captoPRIL
-enalaPRIL
-fosinoPRIL
-quinaPRIL
-ramiPRIL
21
Q
use of ACE inhibitors
A
hear failure
22
Q
heart failure ACE inhibitors increase
A
-cardiac output and performance of heart
23
Q
ACE inhibitors in heart failure: improve
A
-hemodynamics
-improve quality of life
-delay mortality
in dogs and cats
24
Q
ACE inhibitors are classified also as
A
vasodilators
25
ACE inhibitors in renal failure: simultaneous administration of ACE inhibitors and diuretics (e.g furosemide) lead to same effect as in case of
simultaneous administration of diuretics and cardiac glycosides > risk of occurrence of hypokalemia or ventricular arrhythmia is higher when glycosides are administered
26
ACE inhibitors in renal failure: combination of for example
captopril-digoxin
27
drug interactions: ACE inhibitors potentiate effect of diuretics, but
-renal flow decreases > (angiotensin 2 maintains glomerular filtration rate, with ACE inhibitors GFR is decreased)
-it can lead to azotemia (plasma urea concentration increases)
28
NSAIDs may diminish effect of
ACE inhibitors
29
side effects of ACE inhibitors - relatively safe for
dogs
30
ACE inhibitors side effects: vomiting,
diarrhoea and anorexia may be experienced
31
side effects of ACE inhibitors sometimes an excessively sharp and powerful drop
in blood pressure
32
side effect ACE inhibitors hypo..
hypokalemia
33
captopril-bioavailability in dogs after administration through oral route
75%
34
captopril-full GIT tract bioavailability
30%
35
captopril - maximum effect is reached
1-2 hours after administration
36
captopril-primary effect in dogs
vasodilation
37
enalapril-bioavailability of
65%, maximum effect is reached after 2 hours
38
enalapril-duration of effect
12-14 hours
39
enalapril-effect: clinical improvement in dogs with heart failure due to
dilated cardiomyopathy or mitral regurgitation
40
lisinopril-bioavailability of
25-50%, fullness of GIT does not impact bioavailability
41
lisinopril-maximum effect is reached
6-8 hours after administration
42
benazepril-bioavailability
increases with repeated dosing, slight accumulation of drug
43
benazepril-for treatment of
congestive heart failure in dogs
44
cardiotonics i.e. cardiac glycosides i.e. digitalis glycosides- by acting on processes regulating cardiac function using cardiac glycosides it is possible to
-strengthen systolic contraction
-increase heart rate per minute
-reduce myocardial oxygen demand
-increase energy resources of heart = glycogen and creatine content of myocardium
45
using cardiac glycosides : such effect can also be achieved using
beta-adrenomimetics (temporarily)
46
cardiotonics-representatives: digitoxin, digoxin and gitoxin- glycosides obtained from
leaves of common foxglove (Digitalis purpurea)
47
cardiotonics- k-Strophanthidin-glycoside obtained from
seeds of Strophantus hispidus
48
cardiotonics-g-Strophanthidin-glycoside of
Strophanthus gratus
49
cardiotonics-Convallatoxin-glycoside extracted from
lily-of-valley (Convallaria majalis)
50
cardiotonics-Scillared-glycoside extracted from
squill
51
cardiotonics-pharmacokinetics depends on
lipid solubility and number of OH groups in structure - breakdown induced by gastric acid
52
digitoxin is absorbed best from
GIT - descending order as follows: digoxin, celanide, strofantin(not absorbed at all-injection)
53
water soluble Digitalis Glycosides (DG) are
injected into vein , onset action is within minutes
54
Digitalis Glycosides (DG) are partially bound to
blood proteins
-digitocin only has on OH group, absorbed well GIT
-strofantin has 5 OH groups , is not absorbed at all
55
DG primarily absorbed
in small intestine subsequent to p.o. administration
56
digoxin and digitoxin are absorbed in dogs and cats
p.o. 75-90% (strofantin 5-10%)
57
DG biotransformation
in liver, excreted through kidneys
-accumulated in addition to heart also in liver, kidneys, GIT
58
digitocin excreted
at slowest rate and strofantin is excreted at fastest rate
59
DG effect is
similar between substances
60
DG have direct impact on
-heart working capacity
-have effect on mechanism and contraction events of cardiac muscle, its excitation
61
DG normalise
-oxygen demand of myocardium
-as result of that-performance of heart increases
62
DG reduce activity of
K-Na-ATPase
63
DG result of K-Na-ATPase activity reduction
-concentration of extracellular K and intracellular Na increase
-concentration of intracellular Ca increases
-strengthening and quickening systolic contraction of heart and POSITIVE INOTROPIC effect occurs
64
DG reflexive mannes ....effect occurs
negative chronotropic effect occurs
-irritation of aortic arch and carotid sinus receptors due to strengthen pulse induces bradycardia throug vagus nerve
65
DG extracardiac effect
-increase diuresis
-due to faster blood circulation
-blood supply of kidneys improves
-diuresis increases
-swellings resolve
66
DG relocation of
-blood in organism
-part of blood relocated cardiac blood pool organs
-abdominal cavity blood vessels
-cardiac load decreases
67
DG toxicity, side effects: humans experience
central nervous system effects:
hallucinations, psychosis, delirium, coma, yellow vision disturbances, lack of appetite, nausea, vomiting
68
DG vomiting id both in animals and humans caused by
direct irritation of trigger zone of 4th ventricle of brain
69
DG cardiac effect: side effect
-blocked impulse transmission
-extrasystoles
-ventricular fibrillation
-AV block
70
DG toxicity : dogs primarily experience
irritation of GIT, loss of body weight, life-threatening arrhythmia, anorexia and vomiting
71
DG (Digitalis Glycosides) if toxic reactions appear
-treatment should be terminated
-it may be necessary to administer K into vein
72
DG primarily used in
small animals and horses
73
DG indication
heart failure
74
DG some treatment regimes, initially a loading dose is
administered i.e. so-called digitalization
- treatment is continued with maintenance dose = 1/5 to 1/8 of initial dose
75
DG indication could be also
atrial fibrillation
76
DG preventive digitalization-before lengthy
heart surgeries, cardiac glycosides may be administered in order to reduce toxicity of anaesthetics
77
DG .... unless weak compared to beta-agonist and amrinone, milrinone
positive inotropic effect
78
DG main effect
diuretic effect
79
DG ... vascular baroreceptor function
increased
80
DG.... sympathetic activity
decreased
81
DG .... increase parasympathetic nerve activity to sinus node, ratio and AV node
anti arrhythmic effects
-used for controlling supra ventricular tachyarrhytmias
82
DG cats are more ... than dogs and require .. doses
-sensitive
-lower
83
DG doses are smaller in case of
liver impairment and kidney impairment
84
DG contraindications are shock from loss off
shock from loss off blood , liver impairment and kidney impairment, ventricular arrhythmias
85
non-glycoside inotropic agents : Bipyridine derivatives
lisää lihaksen supistumisvoimaa
86
amrinone- non-glycoside inotropic agents: ...effect
positive inotropic effect= lisää sydämen supistumisvoimaa
87
amrinone gives
stronger heart rate
88
amrinone heart rate does not
increase
89
amrinone-O2 requirement of cardiac muscle is
reduced
90
amrinone used for
short-term inotropic support in small animals with myocardial failure
91
milrinone .... more potent than amrionen - effect ..
-20-30x
-similar
92
milrinone contraindication - unsuitable for
chronic heart failure, side effects occur
93
cardiac stimulants : (2)
-beta-adrenomimetics
-methylxanthines
94
cardiac stimulants: heart contraction power
increases and positive inotropic effect occur (stronger heart muscle contraction)
95
cardiac stimulants-cardiac energy resources
are used up more quickly-duration of action short-followed by complete exhaustion
96
cardiac stimulants-used in case of
acute heart failure-for energizing animals on short term basis that have been sick for long period of time
97
adrenaline-it stimulates
beta-adrenorreactive systems
-has positive chronotropic and inotropic effect (nostaa sydämen sykettä ja voimistaa sydänlihaksen supistumista)
98
adrenaline- heart becomes
-quicker, performance increases, O2 req. of heart increase
-ventricular irritability increases, extrasystoles and fibrillation may occur
99
dopamine (cardiac stimulants) precursor for ..., decreases ...., increases ....
-noradrenaline
-ventricular filling pressures
-cardiac output
100
dobutamine (heart stimulant) synthetic ...., ... effect
-catecholamine
-inotropic
101
caffeine, euphylli, aminophylline-methylxanthines : they have .... and .... effect
positive chronotropic and inotropic
=ventricular contraction strengthens, systole becomes more powerful
-rapid onset and duration of action is short
102
methylxanthines-were used in
heart failure
> failures caused by infectious disease > as stimulant for CNS in case of general weakness
(not animals)
103
analeptics:
heptaminol, diprophyllin, diprophyllin
104
supportive treatment of acute cardiovascular and/or respiratory insufficiency (analeptic treatment)
heptaminol + diprophyllin
105
cardiovascular analeptic
heptaminol
106
heptaminol-action is related to
peripheral release of norepinephrine
107
heptaminol ... blood flow in aorta and has .... and .... effect > especially in case of weak heart work. ... corona blood flow
-increases
-positive inotropic and chronotropic action
-increases
108
diprophyllin (methylxantin) is
fosfodiesterase inhibitor , derivate of theophylline
109
diprophyllin has .... and ... action
analeptic and ccardiorespiratory
110
diprophyllin relaxes...,dilates..., stimulater ... and ..., and increase
-bronchospasms
-coronary arteries
-respiration and cardiac work
-blood flow to heart
111
antiarrhythmic agents reduce
impulse conduction system automaticity > activity of impulse origins outside sinus node is reduced and rhythm of heart normalizes
112
antiarrythmic agents classified
1-4(5) classes
113
lidocaine, quinidine, procainamide, aim aline, ethmozine, ethacizine
class 1 antiarrhythmic agents
114
class 1 anti arrhythmic agents block .... . impulse conduction
-inflow of Na and Ca into cell
-speed and myofibril excitation decreases
115
class 1 anti arrhythmic agents used for
treatment of acute ventricular arrhythmias but due ti several side effects use is limited
116
propranolol, oxprenolol, atenolol, esmolol
class 2 anti arrhythmic agents
117
class 2 antiarrhthmic agents basis of mechanism of action of
beta-adrenergic blocking agents is to block effect of catecholamines on impulse generation and impulse conduction of heart, reducing flow of Na ions into cell
118
class 2 anti arrhythmic agents cardiovascular system effect is varied
-direct beta-adrenergic blockade
-stabilising effect of membranes
-selective effect on various tissues
119
class 2 anti arrhythmic to treat
supraventricular and ventricular arrhythmias
120
class 3 anti arrhythmic agents
-solatol
-amiodarone
121
class 3 anti arrhythmic agents suppress
rhythm disorders caused by excess of catecholamines and having antiadrenergic effect
122
class 3 anti arrhythmic agents do not impact
ion transport
123
class 3 anti arrhythmic agents lower
blood pressure
>increase fibrillation threshold, are used to prevent sudden death due to ventricular arrhythmias
124
class 4 anti arrhythmic agents
-verapamil
-nifedipine, amlodipine
-diltiazem=for slowing ventricular rate in case of atrial fibrillation
125
class 4 anti arrhythmic agents are ... blockers
calcium channel blockers
126
class 4 anti arrhythmic agents suppress
permeation of Ca into cells > reducing cardiac muscle contractility and heart rate normalizing rhythm, blood vessels dilate
127
class 4 anti arrhythmic agents do not impact
Na-K ion exchange
128
class 4 anti arrhythmic agents treatment
paroxysmal supraventricular tachycardia
129
pimobendan- derivative of
benzimidazole-pyridazinone is non-sympathomimetic, non-glycoside inotropic agent that has potent vasodilatory effect
130
pimobendan used in dogs in treatment of
congestive heart failure caused by dilated cardiomyopathy or valvular disease (mitral regurgitation and/or tricuspid regurgitation)
131
pimobendan has .... and positive... -inodilator
vasodilator and positive inotropic
132
levosimendan increases
calcium sensitivity to myocytes by binding to troponin C in calcium dependent manner
-increases contractility without raising calcium levels
133
levosimendan relaxes
vascular smooth muscle by opening adenosine triphosphate sensitive potassium channels
134
levosimendan is used to manage
acutely decompensated congestive heart failure
135
substances that cause dilation of blood vessels
-prazosin (alfa 1-blocker)
-nitroglycerin
-nitroprusside
-captopril
-enalapril
136
dilation of blood vessels : propentofylline : peripheral .... increases
-vasodilator
-increases flow of blood into brain, as well as cardiac and skeletal muscle > this inhibits aggregation of blood platelets and improves flow properties of erythrocytes
137
propentofylline used to improve
cerebral blood circulation and peripheral blood supply in dogs, administered in tablet form
138
amlodipine: treatment of
systemic hypertension in cats
139
amlodipine is a
voltage dependent calcium-channel blocker that is part of dihydropyridine group, selectively binding to L-type calcium channels in smooth muscle of blood vessels, cardiac muscle and cardiac nodal tissue
140
amlodipine prefers L-type
calcium channels in smooth muscle of blood vessels, thereby lowering vascular resistance
141
primary blood pressure-reducing effect of amlodipine is derived from
its direct relaxant effect on arteries and arterioles
142
effect of amlodipine on venous blood circulation
is low
143
amlodipine ... effect endures and decreases depending upon dose
antihypertensive
144
