Cardiovascular (year 2) Flashcards
what may want to be affected using cardiac pharmacology? (7)
heart rate/rhythm contractility relaxation of ventricles preload afterload perfusion arterial pressure
what do positive inotropes do?
increase contractility
what do negative inotropes do?
decrease contractility
what do positive lusiotropes do?
increase relaxation
what do negative lusiotropes do?
decrease relaxation
what do positive chronotropes do?
increase heart rate
what do negative chronotropes do?
decrease heart rate
where is cardiac rate controlled?
cardiovascular centre in the medulla oblongata
what nervous system controls the cardiac rate?
autonomic nervous system
what is conduction of cardiac action potentials reliant on? (3)
normal Na, K, Ca channels
normal intra/extracellular Na, K, Ca levels
functioning interacted discs
what do tachyarrhythmias decrease?
diastolic filling time and hence cardiac output
what does increased cardiac work result in?
myocardial hypertrophy
what can be done to treat tachyarrhythmias? (2)
reduce firing rate
slow conduction of impulses
what are the classes of antidysrhythmics?
I II III IIII miscellaneous
what do class I antidysrhthmics block?
sodium channels
what do class II antidysrhthmics block?
beta blockers (beta1)
what do class III antidysrhthmics block?
potassium channels
what do class IV antidysrhthmics block?
calcium channels
what sodium channels do class I antidysrhythmic block?
fast
where are fast sodium channels present?
cardiac myocytes (doesn’t effect nodal tissue)
what do class I antidysrhythmic cause?
slower depolarisation
what does use dependant sodium channel blockade mean?
preferentially bind to open/refractory sodium channels over resting ones
why is it significant that class I antidysrhythmics don’t effect nodal tissues?
reduce tachyarrhythmias but doesn’t effect normal heart rates
what do class I antidysrhythmics depend on being normal to function properly?
extracellular potassium (hypokaleamia reduces function)
