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Biology 219 – Human Physiology
Clemens
Cardiovascular System 2 – Cardiac Function
Text: Ch. 14
A. Cardiac Cycle
systole - contraction phase (ventricular systole ~1/3 of cycle)
diastole - relaxation phase (ventricular diastole ~2/3 of cycle)
5 specific phases of cardiac cycle
(1) ventricular filling (mid to late diastole):
low P in ventricle
AV valves open, semilunar valves closed
ventricular volume ↑
(2) atrial systole (end of ventricular diastole):
atrial contraction “tops off” ventricles after passive phase of ventricular filling
(3) isovolumic contraction (beginning of ventricular systole)
P↑↑ rapidly as ventricles contract
AV valves close → 1st heart sound (“LUB”)
semilunar valves still closed, so volume stays constant as P increases
(4) ventricular ejection: (mid to late systole):
P↑ to maximal
semilunar valves open
blood ejected to arteries and ventricular volume ↓
(5) isovolumic relaxation (beginning of diastole)
P↓↓ rapidly
semilunar valves close → 2nd heart sound (“DUP”)
AV valves stay closed until ventricular P < atrial P
- Pressure in LV ranges from ~ 0 during diastole to 120 mm Hg at peak of systole.
- Arterial BP in aorta & large arteries ranges from 80 (diastolic) to 120 mm Hg (systolic).
BP is sustained in diastole by closure of semilunar valves and elastic recoil of arteries.
- Volume in ventricles is highest at end of diastole, lowest at end of systole.
Wiggers cardiac output diagram (refer to textbook) correlates:
- electrical events (ECG)
- pressure changes in atria, ventricles, and aorta, volume and heart
- volume changes in ventricles
- heart sounds
B. Cardiac Output
= total blood flow per minute from one ventricle; RV and LV have the same output
cardiac output (CO) = heart rate (HR) X stroke volume (SV)
resting: 5,000 mL/min ≈ 72 beats/min X 70 mL/beat
- CO is total blood flow to all tissues of the body (systemic circuit);
increased demand for O2 and nutrients is accommodated by increase in CO
2. Stroke Volume
end-diastolic volume (EDV) – end-systolic volume (ESV) = SV
(Resting values: 130 mL
60 mL
70 mL )
Control of Cardiac Output
1. Modulation of Heart Rate
a. Autonomic NS
sympathetic: sympathetic cardiac nerve (NE) → β1 adrenergic receptors
→ increased rate of pacemaker depolarization at SA node → increases HR
- E & NE secreted by the adrenal medulla also bind to β1 receptors to increase HR
parasympathetic: vagus nerve (ACh) → muscarinic receptors → decreases HR at SA node
- parasympathetic control dominates at rest (“vagal tone”)
Biology 219 – Human Physiology
Clemens
2. Modulation of Stroke Volume
a. Intrinsic control: Starling’s Law of the Heart
increase in EDV → increase in force of contraction → increase in SV
- results from the length-tension relationship of cardiac muscle:
increased filling stretches sarcomeres to a more optimal part of L-T curve
- EDV increases due to increased venous return to the heart
b. Extrinsic control
sympathetic NS → NE
→ increase in contractility of the heart
adrenal medulla → E & NE
Signal transduction pathway:
1. E and NE bind to β1 adrenergic receptors
2. GPCR activates the cAMP second messenger system → phosphorylation of proteins
3. ↑ Ca2+ entry from the ECF and ↑ Ca2+ release from the SR
4. ↑ actin-myosin crossbridge formation → ↑ force & speed of contraction