Heart Phys Flashcards
(22 cards)
major targets of cardiovascular drugs
voltage gated ion channels. anti-arrhythmic, anti-hypertensive, anti-angina.
three major channel conformations
resting (closed), activated (open), inactivated (closed). there is an inactivation gate as well as an activation gate.
phases 0-4 of the major active ionic current
0: depolarization
1: early repolarization
2: plateau
3: repolarization
4: resting (diastole)
slow response action potential
occurs in the nodes (SA and AV). only stages 0, 3, and 4. no plateau.
autonomic control of heart rate
Norepi and Epi increase heart rate (positive chronotropy)
ACh decreases heart rate (negative chronotropy)
threshold for excitation
amount of membrane depolarization required to produce an action potential
what does hypokalemia do to threshold?
hyperpolarizes, increases the threshold. this should decrease excitability, but gk decreases with low potassium causing increased excitability
what does hyperkalemia do to threshold?
depolarizes, decreases the threshold.
sodium current availability
resting membrane potential directly affects cardiac excitability. more depolarizing current required means increase in threshold, and vice versa.
resting membrane potential
can’t be determined by the Nernst equation. determined by the balance of inward Na+ and outward K+ ionic currents. resting myocardial membrane is 20 times more permeable to K than Na ions.
what happens in severe hyperkalemia?
depolarizes Vm, increases threshold through Ina inactivation, and decreases excitability
functional refractory period
minimum time duration after an action potential required for a threshold stimulus to produce a full response again
effective refractory period
no action potential may be elicited no matter how strong the stimulus
relative refractory period
higher than normal stimulus will elicit an action potential with reduced amplitude and duration
3 major determinants of conduction velocity
rate of phase 0 depolarization, resting membrane potential (more negative Vth = faster conduction), threshold potential (less negative Vth = slower conduction)
what is important about AV node delay
critical to ensure that atrial contraction finishes before ventricular contraction begins
contraction
- Ca enter through Ica,L channel
- Ca ions activate the ryanodine receptor
- CaRC releases sarcoplasmic Ca into cytosol and initiates contraction
relaxation
Cytosolic Ca is reduced back to resting levels by the SR Ca ATPase and the sarcolemmal Na/Ca exchanger
sympathetic effects on heart
norepi/epi acts at beta 1 adrenergic receptor. increases cAMP and PKA. Increase IcaL and If. leads to positive chronotropy and increased AVN conduction. Increased IcaL and SERCA leads to positive inotropy and increased Ca sensitivity of contractile filaments
parasympathetic effects on the heart
ACh acts at M2 muscarinic receptor. Decreased cAMP and PKA. activated IkaCh. Decreased Ica,L, If, increased IkaCh, leads to negative chronotripy and decreased AVN conduction. Decreased Ica,L and SERCA leads to negative inotropy and decreased Ca sensitivity of contractile filaments
7 phases of the cardiac cycle
phase 1: atrial contraction
- isovolumetric contraction
- rapid ejection
- reduced ejection
- isovolumetric relaxation
- rapid filling
- reduced filling
heart sounds
S1: closure of the mitral and tricuspid valves
S2: closure of the aortic and pulmonary valves
S3: when audible, occurs early in ventricular filling
S4: when audible, vibration of the ventricular wall during atrial contraction (ventricular hypertrophy)
