Cardiac Output and Heart Rate Regulation

Cardiac Output, Blood Flow, and Blood Pressure

• Cardiac output (CO) is the volume of blood pumped per minute by each ventricle
• Stroke volume (SV) is the volume of blood pumped per beat by each ventricle
• CO = SV x HR
• Total blood volume is approximately 5.5 liters

Regulation of Cardiac Rate

• The sinoatrial (SA) node initiates the heartbeat's rhythm in the absence of neuronal stimulus
• Sympathetic and parasympathetic nervous system activity influence heart rate (chronotropic effect)
• The autonomic innervation of the SA node regulates heart rate
• Sympathetic and parasympathetic nerve fibers modulate spontaneous depolarization

Regulation of Cardiac Rate (continued)

• Norepinephrine (NE) and epinephrine (Epi) stimulate the opening of pacemaker (HCN) channels
• This accelerates SA node depolarization, increasing heart rate (HR)
• Acetylcholine (ACh) promotes the opening of potassium (K+) channels
• The resultant K+ outflow counteracts Na+ influx, slowing depolarization, and decreasing HR

Regulation of Cardiac Rate (continued)

• The cardiac control center in the medulla coordinates the autonomic nervous system
• Sympathetic nerve endings in atria and ventricles can increase the strength of contraction

Effects of Autonomic Nerve Activity on the Heart

• Sympathetic: Increases the rate of diastolic depolarization, and increases cardiac rate. Increases conduction rate in the AV (atrioventricular) node. Increases strength of atrial muscle contraction and ventricular muscle contraction.
• Parasympathetic: Decreases the rate of diastolic depolarization and thus decreases cardiac rate. Decreases AV node conduction rate. No significant effect on atrial or ventricular muscle.

Stroke Volume

• Stroke volume (SV) is determined by three factors:
  • End-diastolic volume (EDV): the volume of blood in the ventricles at the end of diastole
  • Total peripheral resistance (TPR): impedance to blood flow in the arteries
  • Contractility: the strength of ventricular contraction

Regulation of Stroke Volume

• EDV is the workload (preload) on the heart before contraction
• Stroke volume (SV) is directly related to preload and contractility
• Strength of contraction is directly related to EDV
• Total peripheral resistance (afterload) impedes ejection from the ventricle
• Ejection fraction is SV/EDV (normally 60%); a useful clinical diagnostic tool

Frank-Starling Law of the Heart

• The strength of ventricular contraction directly correlates with EDV
• This is an intrinsic property of the myocardium
• Increased EDV stretches the myocardium, which results in stronger contraction
• The law emphasizes the relationship between heart filling and contractility.

Frank-Starling Law of the Heart (continued)

• The state of myocardial sarcomeres immediately before filling is characterized by actin overlap. Myosin interactions are reduced, leading to a weaker contraction
• Increasing interaction of actin & myosin as ventricles fill leads to increased contractile force.

Extrinsic Control of Contractility

• At any given EDV, strength of contraction is dependent upon the level of sympathetic-adrenal activity
• Norepinephrine (NE) and epinephrine (Epi) increase heart rate and induce a positive inotropic effect (increasing the strength of contraction)
• This is due to increased Ca2+ in the sarcomeres.

Venous Return

• Venous return is the return to the heart of blood via veins
• It controls end-diastolic volume (EDV), affecting stroke volume (SV), and cardiac output (CO)
• Venous return depends on blood volume & venous pressure, vasoconstriction stemming from the sympathetic NS and skeletal muscle pump activity
• Inhaling reduces venous pressure.

Venous Return (continued)

• Veins carry most of the blood volume (approx. 70%) in the body, they are referred to as capacitance vessels. Walls are thin and thus highly compliant.