Cardiovascular System: The Heart
What is the normal activation pattern of the heart
An AP initiaties in the SA Node...propagates throught the atrial muscle (atria contract)...arrives at AV node...AP propagates rapidly down the AV bundle and through the left/right branches...and reaches the Purkinje fibers...APs are then triggerd in ventricular muscle and contract ventricles
Fast response APs are seen in
atrial and ventricular muscle cells
what are the features of fast response APs
rapid upstroke...long lasting deplarization (plateau phase)...rapid repolarization...no depolarization between APs
Slow response APs are seen in
cells within the SA node, AV node, conducting bundles, and Purkinje cells
what are the features of slow response APs?
rapid rise...no plateau pahse...slowish repolatization...slow depolarization between APs called diastolic depolarization
what is the lowest that the membrane potential ever reaches during diastole?
maximum diastolic potential
what causes the rapid rise phase in the atrial and ventricular muscle?
what cause the plateau phase in the atrial and ventricular muscle?
the opening of L-type Ca channels
what cause the repolarization pahse in the atrial and ventricular muscle?
closing of L-type Ca channel and opeing of K channels
what is the force generated by ventreicular muscle known as
what are factors that affect contractility called?
Positive inotropic effects...increase contractility
Negative inotropic effects...decrease contractility
what is the primary influence on contractility?
the SNS...the PSNS does not innervate muscle tissue
what is another name for the diastolic depolarization phase?
known as funny channel (If channel)...it opens during the diastolic period and cuases a steady influx of Na
The property where the heart can trigger its own APs without and external input is known as
what is the key property that enables autorythmicity?
funny channels are found in SA node, AV node, conducting system, and Purkinje fibers, but not in?
atrial and ventricular muscle
why is the SA node considered the pacemaker?
it has the highest number of funny channels and therefor has a faster diastolic depolarization
what is is called when the heart is driven by a pacemaker other than the SA node?
what are three mechanisms for changing heart rate?
increase the number of funny channels (increase heart rate)
increase mazimum disatolic potential (decrease heart rate)
increase threshold for L-ype Ca (decrease heart rate)
the PSNS uses the three mechanisms (deactivate L-type Ca, open K channels to hyperpolarize cell, and decrease number of funny channels) in order to?
decrease the heart rate
The SNS increase the number of funny channels, and increses the number of Ca channels in order to?
increase heart rate
the period of active contraction of ventrical muscle
the period of relaxation of ventrical muscle
when ventricles are relaxed and willing with low-pressure blodd from atria
the phase of the cardiac cycle when the ventricles start to contract, but the volume isnt changing
isovolumetric contraction (beginning of systole)
ejection phase (end of systole)
when ventricular pressure exceeds aortic pressure and blood is ejected into the aorta
when the ventricular pressure starts to drop, but volume does not change
what is the term when the aortic pressure shows a brief upward deflection?
what is the pressure that drives blood flow through the vascular system?
what is a reduction in the elasticity of arterial walls called
this is a condition where the arotic valve is hardened and thus has a high resistance
the distance between the L and R iosvoumetric parts
the "external work" done by the heart during a cycle is
the area bewlow the top curve=systolic work
the area below the bottom curve=diastolic work and the net work is the difference between systolic and diastolic work
this occurs when the ejection curve intersects the systolic prseeure curve
aortic valve closure
what does it mean when cardiac output is self-regulating
if CO increases...intrinsic feedback mechanisms will bring it down and vice versa
positive inoropic effects due to contractility are known as
negative inotropic effects due to contractility are known as
what is mean systemic filling pressure (MSFP)
It is the maximum possible RAP of stationary blood filling the CV system
typical value is 7mmHg
what are two factors that affect the vascular function curve?
blood volume and arteriole tone
what are two ways in which blood volume can be altered?
increase venous tone (squeeze blood out of veins or blood transfusion)
what are the three key concepts regarding steady state CO?
1. output of CO must equal input or vascular return to heart
2. high RAP=high CO, but low venous return and vice versa
3. an imbalance between CO and venous return will change RAP
what is the poitn where teh two curves (cardiac and vascular curves) intersect known as
three things that affect CO
1.increase blood volume...increase CO
2.positive inotropic effects (increase contractility)...increase CO
3. increase in arteriole tone...decrease in CO and vice versa