Cardio Lec 4 Flashcards
Normal heart sounds
s1, s2
s1 due to
av valve closing (ventricular systole)
s2 due to
semilunar valve closing (ventricular diastole)
Heart murmurs
abnormal heart sounds; most often when valve isn’t closing properly so blood is regurgitating due to back flow
When would you hear the murmur
when valve should be closed
During which phase would a murmur due to mitral valve regurgitation be heard most clearly?
during ventricular contraction
Incompetent valves refers to
improper closure (heard as a murmur)
Incompetent valves is due to
damage to papillary muscles or chordae tend.
Does cardiac muscle beats w/o help on NS?
yes
2 types of cells in myocardium
nodal cells & contractile cells
Nodal cells aka
pacemaker cells
T/F Nodal cells have unstable resting membrane potentials
T (have to fire spontaneously/don’t rely on a signal)
What allows heart to beat on own & how
pacemaker cells; nodal cells spontaneously depolarize –> fire an action potential –> send wave to contractile cells –> cause them to depolarize to threshold –> get them to fire action potentials –> heart muscle shortens & contracts
Myocardium connected via
gap junctions
How does wave spread thru heart as a SINGLE UNIT
by all cells being coupled to one another
Atria & ventricles separated via
fibrous skeleton that insulates electrical activity
Impulse that starts cycle originates in the
atria near SVC thru SA node aka pacemaker
Why is the SA node the pacemaker?
bc it fires more frequently than other areas
Do nodal cells contract?
no; they send electrical impulses to contractile cells
T/F: Nodal cells depolarize RAPIDLY on their own
F; SLOWLY
Pacemaker potential refers to
rate of rise to threshold
Funny current/Na channel opens when ___; other ion channels open when ___
membrane potential is most negative; most positive
Describe the action potential prod. by nodal cells/ pacemaker
(before threshold) Na channel opens @ -60 (its most negative) -> some depolarization -> causes transient Ca channel to open -> allows Ca & Na to enter -> 2 channels stay open until threshold -> @ threshold, voltage gated Ca channels open -> other 2 channels shut off -> membrane potential RAPIDLY depolarized -> @ peak, all (+) channels close -> K channels open -> cell repolarizes back to -60 -> funny current opens (little depolarization) -> causes t-type Ca channel open -> the 2 depolarize cell to threshold -> cause voltage gated Ca channels to open -> depolarize to peak -> all shut -> K channels open -> start over & over
What dictates the HR?
rate/ how FREQUENTLY action potentials occur
What would happen if you have a drug that causes channels not to open as fully?
take longer to depolarize –> hr slow down
When the cell is firing its action potential that wave of depolarization spreads to
the adjacent cells via gap junctions
What causes the myocytes to depolarize to threshold?
the spread to the adjacent cells via gap junctions
Pacemaker potential/rise to threshold aka
phase 4
Anything that increases slope of phase 4 will
increase hr
Anything that decreases slope of phase 4 will
decrease hr
Substances that increase slope of phase 4
Epi, norepi (bind to beta1 rs & make it QUICKER to get to threshold)
Substance that decrease slope of phase 4
ACH (makes it take LONGER to get to threshold)
How do substances binding to beta1 rs increase hr?
increase prod. of cAMP which causes Ca channels & funny current to open -> depolarize faster by bringing more + ions in
How does Ach decrease hr?
closes na & ca channels, opens k channels
If Ach given in a high enough does it will
stop the heart as a result of closing of channels
Which would be expected to result in a reduction in hr?
opening of k channels
In pacemaker cells, what ion channels open most dramatically once threshold voltage is reached?
calcium channels
Ectopic foci/pacemaker refers to
any area other than SA node that is pacing the heart
T/F: The SA node is the only nodal area w/ ability to spontaneously depolarize on its own
F; all nodal areas have the ability BUT DO SO LESS FREQUENTLY
T/F: If SA node isn’t working properly, AV node can take over & pace the heart
T but hr would be slower (50-60bpm)
If AV node blocked
Perkinje fibers can take over & pace ventricles but firing rate rlly infrequent; person would have hr: 30bpm -> person needs pacemaker
If area other than SA node or any nodal area is pacing the heart, hr would be
higher
What is required for muscle shortening/contraction?
calcium
Myocardial action potentials initiated by
impulses from pacemaker cells
Ventricular myocyte action potential
cell at RMP (-90 mv) -> depolarization coming from nodal/pacemaker cells -> myocytes to threshold causes na channel to open -> na rushes in & RAPID depolarization -> na channels shut at peak -> k (out) & ca channels open (ca in) -> plateau phase -> ca channels shut -> k channels stay open -> cell re-polarizes
Cannot get contraction until __ because
plateau phase bc ca must be present
When myocytes fire action potentials it causes
myocytes to contract based on ca coming in
Arrythmias/Disrrythmias
abnormal rhythms
What do Na, beta, K, & Ca channel blockers do
slow hr
Cardiac conduction system
SA node signals atria to contract -> signal to AV node (slowly to allow ventricles to fill) -> thru bundle of his -> down bundle branches -> to perkinje fibers (quickly) -> cause ventricles to contract
Cardiac conduction system seen thru
ekg
Only way for signal to get from atria -> ventricle is thru
av node
Excitation contraction coupling refers to
how the myocyte action potential is coupled to the actual contraction of the myocyte
What causes the SR to release its calcium
calcium coming in when the action potential fires in the ventricular myocytes & voltage gated channels open (calcium induced calcium release)
Initial calcium comes from
extracellular sources via VGCCs during plateau phase
Extracellular calcium triggers
release of further intracellular calcium from SR -> causes contraction
