Regulation of Heart Rate
– Heart maintains its own rhythm
– Sinoatrial node (SA node)- stimulus for heart action-
the “pacemaker”
– SA node signal sent to both atria and to
Atrioventricular node (AV node)
* 0.10 sec delay to allow blood to pass from atria into
ventricles below
Regulation of cardiovascular system
-AV node gives rise to the AV bundle (Bundle of His)
- transmits signal via Purkinje fibers (very fast
impulses, 0.06 sec) to ventricles for contraction
* Transmission of cardiac impulse:
SA node → Atria → AV node → AV bundle → Ventricles
what does SA and AV node do in the heart
SA node generates impulse
AV node conducts impulse to
ventricular mass
regulation of the cardiovascular system
cardiovascular control center:
-located in the medulla in the brainstem
egulates:
– heart’s output (SA and AV Node input)
– distribution of blood in the body (viscera, muscle,
etc.)
– vasomotor tone in active muscle (vasoconstriction,
vasodilation)
autonomic nervous system
parasympathetic and sympathetic
sympathetic
Catecholamine
release (epinephrine
& norepinephrine)
* Leads to tachycardia
(HR > 100 bpm)
parasympathetic
Acetylcholine release
* Leads to bradycardia
(HR < 60 bpm)
rest and digest
athletes (endurance) will typically be more bradycardic
sympathetic nervous system
-increase vasoconstriction
-increase vasodilation
-increase contractility (inotropic effect)
-increase heart rate (chronotropic effect)
parasympathetic nervous system
-decrease heart rate
-decrease contractility
-decrease vasodilation of the arterioles of skeletal muscle
-decrease vasoconstriction of visceral arterioles
what nervous system is stimulated when we exercise and what is inhibited?
stimulated =sympathetic inhibited= parasympathetic
resting membrane potential (RMP) of skeletal muscle =
more negative on inside,
more positive on outside
depolarization
membrane potential becoming more positive (influx of sodium)
* Action potential = contraction
systole
contraction
repolarization
membrane potential becoming more negative, back towards resting (efflux of potassium)
relaxation (diastole)
ECG
measures of the hearts electrical activity detected as voltage changes with the ECG
ECG P wave
atrial depolarization
ECG QRS complex
ventricle depolarization (systole)
-often masks atrial repolarization
ECG T wave
ventricle repolarization (diastole)
why is QRS such a big electrical change
the ventricles are much bigger so there needs to be much more electrical activity
what is it - ventricular depolarization not atrial
which electrical activity represents a persons pulse
calculating HR via ECG strip
step 1
calculate distance the paper travels in 1 minute. (paper speed is 25mm/second)
so in one minute the paper traveled 1500mm/min (25mm 60sec/min)
calculating HR via ECG strip
step 2
measure the distance between 4 cycles
one box =5mm,
4 cycles = = boxes mm
blood volume
blood volume in blood vessels is normally 5L
-fully dilated, vessels could hold 20L
arterioles are surrounded by smooth muscle
-innervated by sympathetic neurons, which cause vasoconstriction or vasodilation
blood flow : vasoconstriction and vasodilation
central control (VC and VD)
-peripheral control (metabolic by-products cause VD)
-nitric oxide
autoregualtory mechanism detect metabolic by products reflecting elevated metabolism and the need for more O2