CARDIAC PATHOPHYSIOLOGY Flashcards

1
Q

what is hypertension?

A

disease caused by a sustained blood pressure
usually asymptomatic

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2
Q

what are the different types of hypertension?

A

essential or primary hypertension

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3
Q

what is blood pressure determined by?

A

heart rate, stroke volume, systemic vascular resistance

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4
Q

what is heart rate determined by?

A

autonomic activity

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5
Q

what is stroke volume determined by?

A

preload and afterload) and contractility

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6
Q

what is systemic vascular resistance?

A

‘aggregate vascular tone of arteriolar control of the systemic circulation’

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7
Q

equation of blood pressure?

A

hear rate * stroke volume * systemic vascular resistance

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8
Q

what is normotensive and hypertensive blood pressure maintained by?

A

Cardiac output
Systemic (peripheral) vascular resistance
Venous capacitance
Volume of intravascular fluid (kidney function)

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9
Q

what are the causes in hypertension?

A

complex interaction between environmental and genetics
hypertension related genes regulate renal salt and water handling
believed to activation of the sympathetic nervous system and renin–angiotensin–aldosterone system
Endothelial dysfunction, increased vascular
reactivity, and vascular remodelling

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10
Q

what are cardiac function related effects?

A

pump-based hypertension- increased cardiac output

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11
Q

what are main mechanisms of cardiac function related effects?

A

high levels of activity and increased sensitivity of the heart to basal levels of regulators of SA node contractility

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12
Q

what is used to treat hypertension with cardiac function related effects?

A

B-antagonists

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13
Q

what is vascular function related effects of hypertension?

A

increased systemic vascular resistance

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14
Q

what are renal function related effects?

A

too much Na+ and H2O retention in kidney causes volume based retention

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15
Q

what is a haemodynamic profile?

A

both cardiac output and systemic vascular resistance are elevated caused by Increase in vasomotor tone and Na+ and
H2O retention

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16
Q

what is neuroendocrine related hypertension effects?

A

heart rate and blood vessels effected
abnormal responses to signals
too much production of hormones that regulate circulation

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17
Q

how is Arteriolosclerosis caused?

A

increased blood pressure damaged endothelium
influx of plasma proteins causes hyaline arteriosclerosis

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18
Q

what are the symptoms of arteriolosclerosis?

A

vascular remodelling
thickening of vessel wall
decreased lumen

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19
Q

what happens when hypertension occurs in arteries?

A

Accelerated atherogenesis
increased risk of aortic dissecting aneurism

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20
Q

what is Accelerated atherogenesis?

A

‘distinct lesions at specific sites in
arteries’

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21
Q

how is hypertension treated?

A

counselling and lifestyle changes

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22
Q

what are diurerics?

A

Inhibit Na / Cl transporter and reabsorption
decrease in intravascular volume
decreasing blood pressure
lowers cardiac output

22
Q

what are the pharmacological ways to control hypertension?

A

Reduction of intravascular volume with diuretics
Down-regulation of sympathetic tone (β-antagonists, α1-antagonists)
using calcium channel blockers
ACE inhibitors, AT1 antagonists for Inhibition of the neuro-humoral regulators of the circulation

22
Q

what adrenergic inhibitors are used?

A

β-adrenoceptor antagonists (heart)
α1-adrenoceptor antagonists (blood vessels)
central sympatholytic

23
Q

what are adrenergic inhibitors for?

A

they either reduce cardiac output or reduction of systemic vascular resistance causing negative chronotropic and inotropic effects

23
Q

what do β-adrenergic blockers do?

A

block adrenergic receptors
decrease in heart rate
decrease in inotropy
decrease in sympathetic vasoconstriction

24
Q

what do a-blockers do?

A

Block a-1 adrenergic receptors in smooth muscle
vasodilation occurs due to the reduction of sympathetic stimulation

25
Q

what do ACE inhibitors do?

A

‘Prevents conversion of angiotensin I to
angiotensin II
prevent vasoconstriction associated with angiotensin II’

26
Q

what do AT1 antagonists do?

A

interferes with the binding of angiotensin II to ΑΤ1 receptors
reduction of arteriolar intimal proliferation

27
Q

what do calcium channel blockers do?

A

lower blood pressure through cardiac output and systemic vascular resistance
haemodynamic effects
(acts as a arterial vasodilators
acts as a negative inotropes
acts as a negative chronotropes, which block movement of Ca2+ causing vasodilation)

28
Q

what is cardiac arrhythmias?

A

condition where there’s abnormal electrical activity in the heart

29
Q

what is ECG?

A

repolarization and depolarization of the heart

30
Q

what is the autonomic nervous system?

A

sinus node that controls heart beat

31
Q

what is a normal fast heart beat called?

A

sinus tachycardia

32
Q

what is a normal slow heart beat called?

A

sinus bradycardia

33
Q

when is tachycardia and bradycardia pathological?

A

if tachycardia and bradycardia sustained or linked to feeling dizzy then then it can be pathological

34
Q

what is the P wave generated by:

A

atrial depolarization

35
Q

what is the QRS wave generated by?

A

ventricular depolarization

36
Q

what is the T wave generated by?

A

ventricular
repolarization

37
Q

what is the PR interval a measure of?

A

conduction from atrium to the ventricle

38
Q

what is QT a measure of?

A

duration of ventricular action potential

39
Q

what is flutter?

A

when atria and ventricles are affected with rapid beating

40
Q

what is fibrillation?

A

beats are so rapid that they can’t be measured
can effect both atria and ventricle and lead to cardiac arrest

41
Q

what are the causes of dysfunction in the heart?

A

defect in impulse formation
defects in impulse conduction

42
Q

what is defects in impulse in impulse formation?

A

SA-node working automatically stops leading to missed beats and other areas of myocardium setting their own pace

43
Q

what is arrhythmia?

A

in conduction
effects AV node
slows electrical impulses

44
Q

what is the order of cardiac automaticity?

A

SAN (60-100 bpm) – AVN (40-60 bpm) – myocardium (30-40 bpm)

45
Q

what is re-entrant circuit?

A

‘one of the branch electrical conduction pathways is pathologically disrupted’

46
Q

what are Na+ and Ca2+ channel blockers for?

A

alteration of threshold potential

47
Q

what are K+ channel blockers for?

A

increase the duration of action potential

48
Q

what are Class l antiarrhythmics?

A

‘Na+ channel blockers so (Reduce slope and peak of action potential)’

49
Q

what are Class II antiarrhythmics?

A

’ β-adrenergic receptor antagonists (Reduce rate and conduction)’

50
Q

what are class lll?

A

‘K+ channel blockers (Delay repolarization and increase action potential duration)’

51
Q

what are Class IV antiarrhythmics?

A

‘Ca2+ (L-type) channel blockers (Reduce rate and conduction)’