Flashcards in Ch 13/14 Cardiovascular Physiology (Day 2) Deck (32):
Anatomy of the Heart
-->see slide image
Between atria and ventricles (ensures one-way blood flow)
-Tricuspid valve on the right side
-Bicuspid valve, or mitral valve, on the left side
Between ventricles and arteries (ensures one-way blood flow)
AV valves (tricuspid, bicuspid/mitral) closed
Semilunar valves (pulmonary/aortic) open
AV (tricuspid, bicuspid/mitral) valves open
Semilunar valves (pulmonary, aortic) closed
pump generating driving pressure for blood flow through the circulation
-Heart generates pressure when it contracts (systole) --> pumping blood into arteries
-Arteries maintain pressure by acting as an elastic pressure reservoir between cardiac contractions (i.e. during diastole)
Pumping is periodic, i.e. cardiac activity characterized by cycles of active pumping (systole) followed by resting (diastole).
Pressure changes during cardiac cycle
1) Ventricles begin contraction, pressure rises, and AV valves close (lub); isovolumetric CONTRACTION
2) Pressure builds, semilunar valves open, and blood is ejected into arteries. (pressure of ventricles is much higher)
3) Pressure in ventricles falls; semilunar valves close (dub); isovolumetric relaxation.
--> Dicrotic notch – slight inflection in aortic pressure during isovolumetric RELAXATION
4) Pressure in ventricles falls below that of atria, and AV valve opens. Ventricles fill (passive).
5) Atria contract, sending last of blood to ventricles (active)
What are the pressure differences between L and R side of heart?
left side is 5-6x higher
volume is NOT changing
lub: closing of AV valves at start of isovolumetric contraction
dub: closing of semilunar valves during isovolumetric relaxation
1) EDV (end diastolic volume) - ESV (end systolic volume) = SV (stroke volume)
2) Ventricle does not eject all its volume—can be altered
pressure has reached a point where the mitral valve closes
pressure the heart is working against
overall work that is being done by the heart
-increases as EDV and ESV get further apart
Cardiac Muscle: Contractile cells
Striated fibers organized into sarcomeres
Cardiac Muscle: Autorhythmic (pacemaker cells)
-Signal for contraction (generate electric signal)
-Smaller and fewer contractile fibers
-No organized sarcomeres
1. contractile cells
2. auto rhythmic (pacemaker) cells
Myocardial muscle cells are branched, have a single nucleus, and are attached to each other by specialized junctions known as intercalated disks (gap junctions).
Electrical conduction in myocardial cells
Auto rhythmic (pacemaker) cells spontaneously fire action potentials. Depolarizations of the autorhythmic cells spread rapidly to adjacent contractile cells through gap junctions.
-difference in action potential patterns determine function
Electrical Activity of the Heart
1. Sinoatrial node (SA node) - “pacemaker”; located in right atrium
2. AV node & Purkinje fibers - secondary pacemakers; slower rate than the “sinus rhythm”
Conduction System of the Heart
1. Action potentials spread via intercalated discs.
2. SA node --> AV node (atrial contraction)
-->pause at AV node so that ventricles contract and THEN ventricles contract (so they don't happen at same time)
3. AV node (base of right atrium) and Bundle of His conduct stimulation to ventricles.
4. In interventricular septum, bundle of His --> right and left bundle branches.
5. Branch bundles --> Purkinje fibers --> ventricular contraction.
Sinoatrial (SA) Valve
-Sets the pace of the heartbeat at 70 bpm
-AV node (50 bpm) and Purkinje fibers (25–40 bpm) can act as pacemakers under some conditions
Atrioventricular (AV) Valve
-Routes the direction of electrical signals so heart contracts from apex to base (i.e. from bottom --> top)
-AV node delay due to slower conduction through nodal cells
Excitation-Contraction Coupling of the heart
1. action potential enters from adjacent cell
2. voltage-gated Ca channels open --> Ca enters cell
3. Ca induces Ca release through ryanodine receptor-channels
4. local release causes Ca spark
5. summed Ca sparks create a Ca signal
6. Ca ions bind to troponin to initiate contraction
-->muscle pre-stretch may help this binding
7. relaxation occurs when Ca unbinds from troponin
8. Ca is pumped back into SR for storage
9. Ca is exchanged w/Na by NCX anti porter
10. Na gradient is maintained by Na/K ATPase
-->diff from skeletal muscle: some Ca coming in from cytoplasmic space
Action Potential: Cardiac Contractile Cell
0. Na channels open
1. Na channels close
2. Ca channels open/fast K channels close
3. Ca channels close/slow K channels open
4. resting potential
Why does tetany NOT occur in cardiac muscle?
Skeletal muscle fiber: refractory period is SHORT compared with duration of contraction
Cardiac muscle fiber: refractory period lasts almost as LONG as the entire muscle twitch.
Action Potential: Pacemaker (Autorhythmic) Cells
-->generate their own action potentials (70 times/min = bpm)
-Slow, spontaneous depolarization; aka “diastolic depolarization” – between heartbeats, inward I(Na+) triggered by HYPERPOLARIZATION --> determines HR
-At −40mV, voltage-gated Ca2+ channels open, triggering action potential and contraction.
-Repolarization occurs with the opening of voltage-gated K+ channels.
-->picks up movement of ions in body tissues in response to this activity.
-Does NOT record action potentials, but results from WAVES OF DEPOLARIZATION
-Does NOT record contraction or relaxation, but the ELECTRICAL EVENTS leading to contraction and relaxation
Waves of an ECG
P wave: atrial depolarization
-->P-Q interval: atrial systole
QRS wave: ventricular depolarization
-->S-T segment: plateau phase, ventricular systole
T wave: ventricular repolarization