Cardiac Cycle Description Quiz

Control of Cardiac Output (COP)

• Sympathetic stimulation increases contractility
• Parasympathetic stimulation has no effect on ventricular contraction due to negligible parasympathetic supply to the ventricles
• Digitalis increases the force of ventricular contraction
• Epinephrine hormone increases the force of ventricular contraction by the same mechanism as norepinephrine

The Afterload

• The resistance against which the blood is expelled
• Equivalent to the arterial blood pressure
• The greater the afterload, the less the cardiac muscle can shorten
• Not important in normal range of arterial blood pressure

The Arteries

• Transport blood from the heart to all organs of the body
• Wall of big arteries contains elastic fibers that expand during systole and recoil during diastole
• Arteries have large radii and offer little resistance to the flow of blood
• Low resistance vessels

Arterial Blood Pressure (ABP)

• The lateral pressure of the blood on the arterial wall
• Systolic blood pressure: 125 mmHg, maximum pressure reached during ventricular ejection
• Diastolic blood pressure: 75 mmHg, minimum pressure reached just before ventricular ejection begins
• Diastole starts at the beginning of late rapid repolarization and repolarization is completed by the end of the first half of diastole

Excitability Changes During Action Potential

• Absolute refractory period: cardiac muscle fiber does not respond to any stimulus during phases 0, 1, 2, and about half of phase 3
• Mechanically, this period coincides with the whole period of systole and the beginning of diastole
• Cardiac muscle cannot be tetanized (sustained contraction)
• Relative refractory period: stronger stimulus than normal is needed to produce an action potential during phase 3 until phase 4

Rhythmicity

• The ability of the cardiac muscle to initiate its own impulses regularly, independent of any nerve supply
• Due to the presence of specialized self-excitable fibers (Nodal Tissue)
• The Specialized Cardiac Excitatory-Conductive System consists of:
  • Nodal Tissue: self-excitable fibers that generate regular impulses (Sino-Atrial node, Atrio-Ventricular node, and Purkinje fibers)
  • Conductive Tissue: fibers that carry the cardiac excitation wave from the atria to the ventricles

Digitalis

• Increases the force of ventricular contraction
• Inhibits Na+ K+ pump, increasing intracellular Na+ and decreasing Na+ gradient across the cell membrane
• Prevents Na+ /Ca2+ exchanger from pumping Ca2+ to the extracellular fluid, leading to increased intracellular Ca2+ and increased force of contraction

The Cardiac Output (COP)

• The volume of blood pumped by each ventricle per minute
• COP = Heart rate (HR) x Stroke volume (SV) = 72 beats/min x 70 ml = 5 L/min in a resting average-sized adult
• Stroke volume: the volume of blood pumped by each ventricle per beat = 70 ml
• Pulse pressure: the difference between systolic and diastolic pressure = 50 mmHg
• Mean arterial blood pressure: the average pressure throughout the cardiac cycle = 90 mmHg

Regulation of Arterial Blood Pressure (ABP)

• Nervous regulation: rapid regulation of ABP through reflexes that act within seconds to hours
• Reflexes include receptors, afferent nerves, center, efferent nerves, and response on effector organs
• Most important receptors include arterial baroreceptors and atrial receptors

Arterial Baroreceptors

• Functions:
  • If ABP rises, the rate of discharge of impulses from baroreceptors increases, leading to decreased sympathetic and increased parasympathetic activity
  • Decreased sympathetic supply decreases heart rate and stroke volume, thus decreasing COP
  • Decreased vasoconstriction (VC) decreases total peripheral resistance (TPR), leading to decreased ABP
  • Antidiuretic (Vasopressin) hormone produces both vasoconstriction and increased water reabsorption by the kidney, increasing plasma volume and venous return, thus increasing COP and ABP
  • Aldosterone hormone increases Na+ reabsorption by the kidney, followed by water, increasing extracellular fluid volume, blood volume, and ABP

The Renin-Angiotensin System

• Causes powerful vasoconstriction of the arterioles, increasing TPR and ABP
• Stimulates the release of aldosterone hormone, leading to salt and water retention by the kidney, increasing plasma volume and venous return, thus increasing COP and ABP
• ACE inhibitors block the conversion of angiotensin I to angiotensin II, decreasing the arterial blood pressure