CARDIAC PATHOPHYSIOLOGY Flashcards
what is hypertension?
disease caused by a sustained blood pressure
usually asymptomatic
what are the different types of hypertension?
essential or primary hypertension
what is blood pressure determined by?
heart rate, stroke volume, systemic vascular resistance
what is heart rate determined by?
autonomic activity
what is stroke volume determined by?
preload and afterload) and contractility
what is systemic vascular resistance?
‘aggregate vascular tone of arteriolar control of the systemic circulation’
equation of blood pressure?
hear rate * stroke volume * systemic vascular resistance
what is normotensive and hypertensive blood pressure maintained by?
Cardiac output
Systemic (peripheral) vascular resistance
Venous capacitance
Volume of intravascular fluid (kidney function)
what are the causes in hypertension?
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
what are cardiac function related effects?
pump-based hypertension- increased cardiac output
what are main mechanisms of cardiac function related effects?
high levels of activity and increased sensitivity of the heart to basal levels of regulators of SA node contractility
what is used to treat hypertension with cardiac function related effects?
B-antagonists
what is vascular function related effects of hypertension?
increased systemic vascular resistance
what are renal function related effects?
too much Na+ and H2O retention in kidney causes volume based retention
what is a haemodynamic profile?
both cardiac output and systemic vascular resistance are elevated caused by Increase in vasomotor tone and Na+ and
H2O retention
what is neuroendocrine related hypertension effects?
heart rate and blood vessels effected
abnormal responses to signals
too much production of hormones that regulate circulation
how is Arteriolosclerosis caused?
increased blood pressure damaged endothelium
influx of plasma proteins causes hyaline arteriosclerosis
what are the symptoms of arteriolosclerosis?
vascular remodelling
thickening of vessel wall
decreased lumen
what happens when hypertension occurs in arteries?
Accelerated atherogenesis
increased risk of aortic dissecting aneurism
what is Accelerated atherogenesis?
‘distinct lesions at specific sites in
arteries’
how is hypertension treated?
counselling and lifestyle changes
what are diurerics?
Inhibit Na / Cl transporter and reabsorption
decrease in intravascular volume
decreasing blood pressure
lowers cardiac output
what are the pharmacological ways to control hypertension?
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
what adrenergic inhibitors are used?
β-adrenoceptor antagonists (heart)
α1-adrenoceptor antagonists (blood vessels)
central sympatholytic
what are adrenergic inhibitors for?
they either reduce cardiac output or reduction of systemic vascular resistance causing negative chronotropic and inotropic effects
what do β-adrenergic blockers do?
block adrenergic receptors
decrease in heart rate
decrease in inotropy
decrease in sympathetic vasoconstriction
what do a-blockers do?
Block a-1 adrenergic receptors in smooth muscle
vasodilation occurs due to the reduction of sympathetic stimulation
what do ACE inhibitors do?
‘Prevents conversion of angiotensin I to
angiotensin II
prevent vasoconstriction associated with angiotensin II’
what do AT1 antagonists do?
interferes with the binding of angiotensin II to ΑΤ1 receptors
reduction of arteriolar intimal proliferation
what do calcium channel blockers do?
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)
what is cardiac arrhythmias?
condition where there’s abnormal electrical activity in the heart
what is ECG?
repolarization and depolarization of the heart
what is the autonomic nervous system?
sinus node that controls heart beat
what is a normal fast heart beat called?
sinus tachycardia
what is a normal slow heart beat called?
sinus bradycardia
when is tachycardia and bradycardia pathological?
if tachycardia and bradycardia sustained or linked to feeling dizzy then then it can be pathological
what is the P wave generated by:
atrial depolarization
what is the QRS wave generated by?
ventricular depolarization
what is the T wave generated by?
ventricular
repolarization
what is the PR interval a measure of?
conduction from atrium to the ventricle
what is QT a measure of?
duration of ventricular action potential
what is flutter?
when atria and ventricles are affected with rapid beating
what is fibrillation?
beats are so rapid that they can’t be measured
can effect both atria and ventricle and lead to cardiac arrest
what are the causes of dysfunction in the heart?
defect in impulse formation
defects in impulse conduction
what is defects in impulse in impulse formation?
SA-node working automatically stops leading to missed beats and other areas of myocardium setting their own pace
what is arrhythmia?
in conduction
effects AV node
slows electrical impulses
what is the order of cardiac automaticity?
SAN (60-100 bpm) – AVN (40-60 bpm) – myocardium (30-40 bpm)
what is re-entrant circuit?
‘one of the branch electrical conduction pathways is pathologically disrupted’
what are Na+ and Ca2+ channel blockers for?
alteration of threshold potential
what are K+ channel blockers for?
increase the duration of action potential
what are Class l antiarrhythmics?
‘Na+ channel blockers so (Reduce slope and peak of action potential)’
what are Class II antiarrhythmics?
’ β-adrenergic receptor antagonists (Reduce rate and conduction)’
what are class lll?
‘K+ channel blockers (Delay repolarization and increase action potential duration)’
what are Class IV antiarrhythmics?
‘Ca2+ (L-type) channel blockers (Reduce rate and conduction)’
