Ninja nerd Cardiac output

Cardiac Output

  • Definition: Cardiac output (Co) is defined as the product of heart rate (HR) and stroke volume (SV).
    Co=HRXSVCo=HRXSV

Heart Rate (HR)

  • Units: Measured in beats per minute (bpm).

  • Normal Range: Typical heart rate ranges between 60 to 100 bpm.

    • Average is approximately 70 bpm.

  • Tachycardia: Defined as a heart rate greater than 100 bpm.

  • SA Node: The Sinoatrial node (SA node) generates and regulates the sinus rhythm, typically maintaining a heart rate of 60 to 80 bpm.

  • Factors Influencing Heart Rate:

    • Sympathetic Nervous System:

    • Increases heart rate through the release of norepinephrine and epinephrine which act on beta-1 adrenergic receptors.

    • This action is termed positive chronotropic effect, enhancing heart rate.

    • Parasympathetic Nervous System:

    • Decreases heart rate via acetylcholine acting on muscarinic receptors, termed negative chronotropic effect.

    • Hormones:

    • Thyroid hormones (T3 and T4) significantly increase heart rate and also metabolic rate.

    • Body Temperature: Higher temperatures typically increase heart rate, while lower temperatures reduce it.

    • Ionic Influence:

    • Calcium: High calcium (hypercalcemia) generally increases heart rate; low calcium (hypocalcemia) decreases it.

    • Potassium: High levels (hyperkalemia) can inhibit heart rate leading to potential cardiac arrest.

  • Chemoceptors Influence:

    • Low blood oxygen (partial pressure), high carbon dioxide (partial pressure), or low pH stimulate chemoceptors, which can also increase heart rate.

  • Age Factor:

    • Fetal Heart Rate: Very fast, typically 120-140 bpm.

    • Adult Heart Rate: Average adult heart rate ranges from 60-80 bpm.

    • Gender Differences:

    • Males (60-72 bpm) vs. Females (72-80 bpm).

Stroke Volume (SV)

  • Definition: The volume of blood ejected by the heart ventricles with each contraction, measured in milliliters (mL).

  • Equation: SV=EDVESVSV = EDV - ESV

    • End-Diastolic Volume (EDV): Volume of blood in the ventricles before contraction, normally around 120-140 mL.

    • End-Systolic Volume (ESV): Volume of blood remaining in the ventricles after contraction, typically about 50-70 mL.

  • Normal Stroke Volume: Average stroke volume is approximately 70 mL per beat.

  • Determinants of Stroke Volume:

    • Preload: The degree of stretch of cardiac muscle fibers just before contraction.

    • Contractility: Strength of contraction influenced by sympathetic stimulation and intracellular calcium levels.

    • Afterload: The resistance the heart must overcome to eject blood; influenced by systemic vascular resistance and aortic pressure.

Preload
  • Definition: Reflects the degree of stretch of cardiac muscle; determined by EDV.

  • Influencing Factors:

    • Increased venous return improves preload.

    • Methods to increase venous return include:

      • Muscle pump: Skeletal muscle contraction helps push blood in veins.

      • Respiratory pumps: Changes in thoracic and abdominal pressure during breathing facilitate blood flow.

      • Vasomotor tone: Sympathetic influence enhances venous return through constriction.

  • Filling Time: Adequate time for heart filling is critical; high heart rates can hinder filling and, subsequently, preload.

Contractility
  • Definition: The ability of the heart muscle to contract.

  • Regulators:

    • Sympathetic nervous system (increases contractility via norepinephrine).

    • Hormones such as thyroid hormones (T3/T4) enhance contractility by increasing receptor expression.

    • Positive Ionotropic Agents: Calcium, epinephrine, norepinephrine, etc., enhance contractility.

    • Negative Ionotropic Agents: Conditions like hyperkalemia and acidosis impede contractility.

Afterload
  • Definition: The resistance the ventricle must overcome to eject blood.

  • Clinically Relevant Issues: Conditions like hypertension increase afterload, making it more challenging to eject blood from the heart.

  • Influences of Afterload:

    • Valvular stenosis or occlusion due to plaque can increase resistance.

    • Increased systemic vascular resistance affects the pressure gradient, increasing afterload.

  • Relationship with Stroke Volume:

    • Increased afterload leads to decreased stroke volume; conversely, decreased afterload improves stroke volume.

  • Clinical Notes:

    • Atrial Bainbridge Reflex: Increased venous return/stretch can stimulate increased heart rate via the cardiac accelerator center.

Conclusion

  • Overview of cardiac output, heart rate, and stroke volume highlights their interrelations, physiological regulations, and clinical implications.

  • Importance of understanding how various factors influence these parameters is crucial for application in clinical settings and understanding cardiovascular physiology.