CARDIO- heart rate and contractility Flashcards
what is heart contractility
strength of a contraction at a given resting load , due to sympathetic nerves and circulating hormones
why would you want to lower heart rate
a higher heart rate is associated with morbidity from cardiovascular disease
what does a high heart rate do
increases myocardial oxygen consumption - heart must work harder
reduces coronary circulation perfusion time
increase risk of arrythmias
linked to atherosclerosis / coronary artery plaque disruption
why would you want to increase heart rate
need to increase cardiac output - hypovolemia, haemorrhage
during excercise
responds to drop in hear rate - MI induced bradycardia which may lower CO
what is the ANS control of heart rate at the SAN - sympathetic
noradrenaline - beta 1 adrenoreceptors GaS- stimulates AC pathway - increases cAMP increase if channel activity increase pacemaker potential frequency increase heart rate positive chronotropic effect
what is the ANS control of heart rate at the SAN - parasympathetic
acetylcholine - M2 receptor GaI_ inhibits AC pathway - decrease cAMP decrease IF channel activity decrease pacemaker potential frequency reduced heart rate negative chronotropic effect
what is the mechanism of action of Beta-1 adrenoreceptor blockers
antagonists - atenolol, bisoprolol
reduce action of the sympathetic nervous system on SAN
lower heart rate
what is a concern of giving beta-1-adrenoreceptor agonists
avoid in asthma patients as may block beta-2- adrenoreceptors
not given with a calcium channel blocker as this can reduce heart rate too much
can produce fatigue
what is the mechanism of action for muscarinic receptor blockers
antagonists - atropine
reduce action of the parasympathetic nervous system (vagus nerve) on SAN
removal of inhibitory influence of vagal tone on heart rate muscarinic receptor blockers - increase heart rate
what are some concerns when prescribing muscarinic receptor blockers
used to treat COPD, IBS, overactive bladder
their condition is likely to have a normal heart rate so may give them tachycardia
tachycardia increases demand on the heart which is bad for patients with COPD
how would you decrease the pacemaker potential frequency at the SAN
inhibit voltage gated calcium channels - reduce phase O, slower upstroke
inhibit if channels - increase phase 4 time, slower to activate calcium channels
what is the mechanism of action for calcium channel blockers
sit in the pore of the channel and block calcium entry into the cell
also found in cardiac myocytes (smooth muscle)
therefore you need to be able to selectively target ca channels in SNA
what are the three subtypes of ca channel blockers and what are the selective for
dihydropyridines (vascular selective)
diphenylalkyamines (cardiac selective)
benzothiazepines ( vascular and cardiac selective)
what is the mechanism of action of if channel blockers
selective inhibitor of if channel in the SAN
reduces pacemaker potential frequency
decreases heart rate to reduce myocardial O2 demand
used to lower heart rate in heart failure patients
ivabradine decreases if channel activity to increase phase 4 time - decrease pacemaker potential frequency and decrease heart rate
outline how increasing intracellular calcium produces an inotropic effect
AP upstroke (Na ions) cause depolarisation of t-tubules - this causes the activation of VCCC, and therefore a calcium influx
the calcium binds to RYR on the SR and triggers more release of ca from SR
this then binds to troponin (as it displaces tropomyosin/troponin complex) exposing the active sites
allows the thick myosin heads allowing binding
ATPase converts ATP-ADP releasing energy
slide filaments = contraction
