CV Physiology Flashcards
Pericardium
Tough inelastic sheath covering heart (anchors heart) Acts as a constraint to enable ventricular interaction Pericardial fluid (lubrication)
Coronary arteries are on
Surface of heart
This prevents compression during contraction
Right atrium receives from and sends to
Receives from vena cava
Sends to right ventricle
Right ventricle receives from and sends to
Receives from right atrium
Sends to lungs
Left atrium receives from and sends to
Receives from pulmonary veins
Sends to left ventricle
Left ventricle receives from and sends to
Receives from left atrium
Sends to body except for lungs
Vena cava receives from and sends to
Receives from systemic veins
Sends to right atrium
Pulmonary trunk (artery) receives from and sends to
Receives from right ventricle
Sends to lungs
Pulmonary vein receives from and sends to
Receives from veins of the lungs
Sends to left atrium
Aorta receives from and sends to
Receives from left ventricle
Sends to systemic artery
Ventricular torsion
Allows for more efficient ejection
Produces diastolic suction (more efficient filling)
Intercalated disks
Desmosomes = withstands stress
Gap junctions = movement of ions, electrical impulses
2 types of myocardial cells
Autorhythmic cells = generates and spreads action potential, pacemaker cells, conducting cells
Myocardial cells = contractile cells, 99% of cardiac cells, mechanical work of contraction
Each myocardial cell has a distinct action potential
Action potentials are initiated at the pacemakers
Heart muscle electrical excitation
Pacemaker cells
Events = Na+ influx, Ca++ influx, K+ efflux
Pacemaker potential = the slow rise in membrane potential (depolarization) prior to an AP in the SA node
Events in pacemaker potential
Slow depolarization phase of SA node = K+ permeability decrease while Na+ increases (increased leakiness to Na+ = slow influx of Na+) approaches threshold
Near midpoint of slow depolarization = Ca++ (T-type; transient) channels open - voltage sensitive, calcium moves in, don’t stay open long, pacemaker potential continues to rise towards threshold
Threshold is reached = L-type Ca++ channels open, calcium moves in, rapid depolarization and action potential
Repolarization = L-type Ca++ channels close, K+ (rectifier) channels open and K+ moves out of SA node cells
SA node is
Autorhythmic
Self-generated
Events repeat (~70 times/minute)
Other pacemaker regions
AV node (40 beats/min) Purkinje fibres (~20 beats/min) (ectopic beats (extrasystoles)) Both are depolarized by SA node before they depolarize themselves
Action potential of myocardial contractile cells
Depolarization (Na+ moves in)
Plateau ( Ca++ moves in, stays depolarized)
Repolarization (K+ moves out)
Cardiac muscle
Excitation-contraction coupling and relaxation in cardiac muscle
Myocardial contractile cells
Long refractory period in cardiac muscle
Long action potential means long refractory period
Prevents tetanus and allows for relaxation and diastolic filling each beat
Modulation of heart rate by the sympathetic nervous system
Pacemaker cells are more depolarized
Closer to threshold
Will reach threshold faster
Increased heart rate
Modulation of heart rate by the parasympathetic nervous system
Hyperpolarizes pacemaker
Further from threshold
Takes longer to reach threshold
Slower heart rate (normal resting condition)
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: membrane potential
Skeletal= stable at -70 mV Contractile = stable at -90 mV Autorhythmic = unstable pacemaker potential, usually starts at -60 mV
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: events leading to threshold potential
Skeletal = net Na+ entry through ACh-operated channels Contractile = depolarization enters via gap junctions Autorhythmic = net Na+ entry through ion channels, reinforced by Ca+ entry
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: rising phase of action potential
Skeletal = Na+ entry Contractile = Na+ entry Autorhythmic = Ca++ entry
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: repolarization phase
Skeletal = rapid, caused by K+ efflux Contractile = extended plateau caused by Ca++ entry, rapid phase caused by K+ efflux Autorhythmic = rapid, caused by K+ efflux
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: hyperpolarizatiom
Skeletal = due to excessive K+ efflux at high K+ permeability when K+ channels close, leak of K+ and Na+ restores potential to resting state Contractile = none, resting potential is -90 mV, the equilibrium potential for K+ Autorhythmic = normally none, when repolarization hits -60 mV the ion channels open again and ACh can hyperpolarize the cell
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: duration of action potential
Skeletal = short, 1-2 msec Contractile = extended, 200+ msec Autorhythmic = varies, generally 150+ msec