Exam 1 Flashcards
What anchors the AV valves and the semilunar valves?
Annulous fibrosis
What valves lie between the atria and ventricles?
Atrioventricular valve
Right - tricupid valve
Lepf- bicuspid or mitral valve
What valve lie between the aorta, pulmonary system and ventricles
semilunar valves
What are the layers of the blood vessel wall?
Tunica intima
Tunica media
Tunic adventitia
Tunica intima
endothelium and elastic lamina
Tunica media
smooth muscle and elastic lamina
Tunica adventitia
connective tissue
What vasculature is distributive?
Elastic and muscular arteries
What vasculature is creates resistance?
Arterioles
What vasculature is for exchange
capillaries
What are the capacitance vessels?
venules and veins
What layer is significant in elastic arteries and what is its effect?
Tunica media with a large amount of collagen and elastin
Windkessel effect- elastic reservoir expanding and recoiling over a cardiac cycle
What is the main layer on muscular arteries? What does it prevent?
Tunica media
Prevents kinking at joints
What is the main layer in arterioles? What controls this?
Tunica media (smooth muscle) sympathetic nervous system and adrenoreceptors (b receptors)
Capillary walls are made of?
single layer of epithelium
What do venules lack?
smooth muscle
What innervates veins? What is the effect of this innervation?
sympatheic nervous system
venoconstricion -> increased CVP -> increased cardiac output
systole
contraction phase
diastole
relaxation phase
heart rate
beat per min
stroke volume
volume ejected per beat
cardiac output
volume ejected per min
pulse pressure
systolic - diastolic
What is resistance
how hard it is for flow (Q) to occur through vessels
What is the major controlling factor of Q?
changes in resistance
What is the calculation for flow (Q)
Q= P / R
What is the equation for resistance (R)
R= 8vL / pi(r^4)
What has the largest effect on resistance
radius of the vessel (r^4)
The sum of all resistances in a series
Total peripheral resistance
Calculatoin for cardiac output
CO= (MAP-CVP) / TPR
The sum of resistances across parallel capillary beds is less than the individual resistance. What does this show about changes in flow across organs?
flow in one organ can be altered without effecting flow of another organ.
flow through an individual bed is dependent on the individual resistance of that bed.
What happens to velocity and pressure when cross sectional area increased across capillaries?
pressure and velocity decrease
What is the physiological pacemaker and where is it located?
Sinoatrial node in right atrium
How does the electrical signal flow through the heart?
SA node -> AV node (slight pause to allow atria to contract) -> Bundle of His in interventricular septum -> Perkinje fibers up sides of heart to myocardium
how does the signal travel quickly in the perkinje fibers
large fibers with many gap junctions
ectopic beat
uncoordinated firing of heart
escape beat
ectopic beat of the ventricles
what is resting membrane potential
-70mV to -90mV
Na+K+ Pump
primary active transport using ATP
transports 3Na+ out and 2K+ into cell to repolarize the cell
Ca2+ ATPase
Primary active transport using ATP to move Ca2+ out of cell.
Na+ Ca2+ exchanger
Uses extracellular Na+ flowing along its gradient (into cell) to pump Ca2+
Secondary active transport
Ligand gated channels
Binding of ligand opens channels allowing flow of ions along gradient causing depolarization/ voltage change
Voltage gated
A change in polarity causes channels to open (flow through gap junctions).
What maintains resting membrane potential
Flow of K+ out (leaky channels)
How are funny currents activated?
Increasing negative voltage
What creates the decaying membrane potential in the SA node
If (funny) currents. Slow efflux of Na+ activated by increasing negative membrane potential
Ca2+ slow influx (voltage gated)
What channels cause the depolarization in the SA node
Ca2+ fast influx channels
What channels repolarize SA node?
K+ fast efflux (ik)
What channels are lacking in the AV node
Fast Na+ channels
How does the excitability of the Av node compare to the SA node?
AV node have slower excitability than SA node.
-slows conduction velocity allowing full contraction of atria
What creates the prominent phase 1 in the action potentials of the atria, bundle of His, purkinje fibers, and ventricular myocardium?
Fast Na+ channels for rapid depolarization
What causes the plateau phase in the ventricular myocyte action potential? What is the heart doing in this stage?
Opening of voltage gated Ca2+ channels.
Ventricular contraction
What is the Pwave?
Activation/ depolarization of atria. Downward direction toward left leg lead -> positive wave
PR interval
Contains P wave and PS segment
Depolarization of R and L atria
PR segment
End of Pwave to beginning of QRS complex
AV node conduction
Q wave
Interventricular depolarization from left to right (away from left leg lead) -> negative defection due to direction
R wave
Ventricular free walls activated
Largest mass depolarizing toward base -> positive wave
S wave
Ventricular activation
Perkins fibers base to apex -> negative direction
T wave
Ventricular muscle repolarization from base to apex (away from left leg lead) -> positive wave
QT interval
Ventricular depolarization, repolarization, and ventricular contraction
ST segment
Isoelectric
Ca2+ influx and contraction of ventricle
U wave
Usually not seen under normal conditions
Possibly due to repolarization of papillary muscles
What condition causes a prominent U wave?
Hyopkalaemia
Why does Hypokalaemia cause changes in the ECG?
Prolonged repolarization due to low K+
Flattened or negative T wave- slow repolarization of ventricles
Prominent U wave - prolonged repolarization of papillary muscles
What are the three ways of determining heart rate from ECG Paper
Count number of boxes between two R waves (calculation)
Count off method (sequence)
Counting number of complexes between the 3sec markers
How does hypertrophy cause changes in the ECG?
Greater electrical current through the expanded chamber (increase voltage)
Chamber may take longer to depolarize (increase duration)
What is Starlings Law?
Cardiac output/ stroke volume will increase in response to an increase in blood filling the heart
Increase preload > increase CO
What is the length-tension relationship of the heart muscle?
Resting cardiac muscle is less than optimal length for tension.
Increase length by increased filling (EDV or preload) => fibers at optimal length creating a greater force of contraction
Increases stroke volume
What happens is the heart is overstretched? What Law applies to overstretched heart?
Heart failure
Law of Laplace
What factors affect preload?
Venous blood pressure -> blood volume and TPR
Rate of venous return (velocity) ->HR and SV
What is afterload?
How hard heart has to work to eject blood
What is the sequence of events due to increased afterload?
Decreased SV > blood left in heart > increase EDV > increased preload > increase muscle stretch (optimal length= increased contractile force) increased volume => increased stroke volume
What does inotropy refer to?
Force of muscle contraction
Name positive inotropes
Noradrenaline
Adrenaline
Angiotensin II
Dobutamine
Name negative Inotropes
B blocker Acidosis Hypoxia Hyperkalaemia Ca2+ channel blockers
What are the autonomic controls stroke volume and where to they act?
Parasympathetic - SA and AV nodes; no ventricular innervation
Sympathetic - SA node and Ventricular myocardium
Explain the process of sympathetic innervation
CNS efferent nerves > ganglion> postganglionic nerves> release noradrenaline > NA agonises B1-adenoreceptors > increase slope of pacemaker potential
Explain the process of parasympathetic innervation
CNS efferent nerves > ganglion > postganglionic PSNS > agonises cardiac m2 muscarinic receptors > decrease Ca2+ influx
