heart cardiac output 2_19

Overview of Cardiac Output

• Cardiac Output: A measure of how well the heart performs its job; defined as the volume of blood pumped by the heart per minute.

• Formula: Cardiac Output = Heart Rate × Stroke Volume.

• A high cardiac output indicates better perfusion of body tissues, enhancing overall function and capacity.

Heart Rate and Stroke Volume

• Heart Rate: Number of times the heart beats per minute, typically between 50-90 bpm at rest.

• Stroke Volume: Amount of blood pumped by the heart with each heartbeat; defines how much blood the heart ejects per stroke.

• Example Calculation: If heart rate is 75 bpm and stroke volume is 70 mL, then Cardiac Output = 75 × 70 = 5250 mL/min or 5.25 liters/min.

Blood Volume

• Average human blood volume is about 4-6 liters.

• At rest, when cardiac output is 5 liters/min, this means the entire blood volume circulates every minute.

Key Concepts Related to Stroke Volume

End Diastolic Volume (EDV) and End Systolic Volume (ESV)

• End Diastolic Volume (EDV): Volume of blood in the heart at the end of relaxation (filling phase); approx. 135 mL in the example.

• End Systolic Volume (ESV): Blood volume remaining in the heart at the end of contraction; approx. 65 mL in the example.

• Stroke Volume (SV): Calculated as EDV - ESV; example gives SV = 135 mL - 65 mL = 70 mL.

• Ejection Fraction (EF): Percentage of blood ejected from the heart; calculated as (SV/EDV) × 100; in example, EF = (70/135) × 100 = 51.85%.

Factors Influencing Stroke Volume

• Preload: Refers to the initial stretch of cardiac muscle; effectively correlates with EDV. More blood returning to the heart increases preload.

• Contractility: Refers to the intrinsic ability of cardiac muscle to contract; can be influenced by norepinephrine and epinephrine. Increased contractility leads to greater stroke volume without changes in EDV.

• Afterload: The resistance the heart must overcome to eject blood; can affect stroke volume.

Mechanisms Affecting Venous Return (Preload)

1. Skeletal Muscle Pump

• Voluntary muscle contraction compresses veins, increasing venous pressure and aiding blood return to the heart.

2. Sympathetic Vasoconstriction

• Activation of sympathetic nervous system causes veins to constrict, increasing venous return by elevating venous pressure.

3. Respiratory Pump

• During inhalation, pressure in the thoracic cavity decreases, which helps pull more blood into the heart via the vena cavae due to pressure differences.

Frank-Starling Law of the Heart

• Describes the relationship between EDV and stroke volume; more filling (preload) leads to a stronger contraction due to increased overlap of actin and myosin filaments within cardiac muscle fibers.

Contractility and Myocardial Function

• Contractility can be enhanced independently from preload; it reflects how forcefully the heart can contract at a specific stretch.

• Physiological modulators like norepinephrine increase intracellular calcium concentration, enhancing the strength of contraction.

Key Takeaways

• Cardiac output is a critical parameter for assessing heart function, determined by heart rate and stroke volume.

• Understanding the roles of EDV, ESV, preload, contractility, and venous return mechanisms is essential for grasping cardiovascular physiology.

• Clinical implications can include conditions of heart failure, exercise physiology, and recovery strategies such as the use of compression garments to aid venous return.