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21 Cards in this Set

  • Front
  • Back
Action Potential at SA Node
Ca ion influx brings it up to -40mV (threshhold)
Autonomic Tone Affecting heart Rate
Dual innervation - sympathetic and parasympathetic
In healthy, resting individuals, parasympathetic effects dominate - Acetylcholine is released
If parasympathetic activity increases, the heart rate declines
If sympathetic activity increases, the heart rate increases
Autonomic Tone Affecting heart Rate - Effects on SA Node
The sympathetic and parasympathetic divisions alter heart rate by changing the ionic permeabilities of cells in the conducting system
Acetylcholine (released by parasympathetic) opens chemically gated K+ channels (positive ions leak out)- this slows the rate of spontaneous depolarization and extends the duration of repolarization so the heart rate slows
Norepinephrine (sympathetic) opens sodium-calcium channels; this influx of positively charged ions increases the rate of depolarization and shortens the period of repolarization so the SA node reaches threshold faster and you get a quicker heartbeat
Action Potential in Cardiac Muscle
See pg. 701
Rapid depolarization - from sodium influx
Plateau - from Ca ion entry
Repolarization - from K ion loss
Skeletal vs. Cardiac Muscle Action Potentials
Skeletal muscle - Action potential and contractiojn are much shorter duration than cardiac muscle
Action Potential

Inhibition
? Postsynaptic potential
Inhibition makes it harder to contract
Arrhythmias
Problems with electrical conduction
Flutter
Fibrillation
Tachycardia
Bradycardia
Arrhythmias

Flutter
200-300 beats/min
Beats are coordinated
Can turn into fibrillation
Arrhythmias

Fibrillation
200-300 beats/min
Beats are uncoordinated
Carn arise from flutter
Arrhythmias

Tachycardia
Greater than 100 beats/min
Arrhythmias

Bradycardia
Less than 60 beats/min
Heart Murmurs
Abnormal heart sounds due to abnormal valve closure
Pressure and Volume changes

Step 1
Atria and Ventricles in diastole - quiescent period; AV valves are open
Semilunar valves are closed
Ventricles have passive filling - over 70% get filled
Pressure and Volume changes

Step 2
Atrial systole
Atria contract and deliver remaining 20-30% of blood to ventricles
End diastolic volume - volume of blood in ventricles at the end of ventricular diastole ( which is when atrial systole ends)
EDV is greatest amount of blood in ventricles
Pressure and Volume changes

Step 3
Ventricles contract (systole)
Increase in ventricular pressure
AV valves close
First heart sound is lub - when AV valves close
Isovolumetric contraction - all valves are closed; pressure increases, but volume doesn't change
Pressure and Volume changes

Step 4
Ventricles still contracting
Semilunar vlaves open
Blood is ejected from ventricles
Pressure and Volume changes

Step 5
Pressure in aorta and pulmonary trunk increase
Semilunar valves close - second sound (dub)
Isovolumetric relaxation - all valves closed; volume stays the same, but pressure in ventricles is decreasing
Pressure and Volume changes

Step 6
Atria are filling and as pressure increase in the atria, the AV vavles open again
Ventricular filling begins again
Blood Pressure
If blood vessels are constricted, total peripheral resistance is increases and blood pressure is increased
If vessels are dilated, total peripheral resistance is decreased and pressure is decreased
Stroke Volume
Amount of blood ejected from ventricles per beat
Heart
see pg 705, 707, 708