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Cardiac output determinants

Cardiac output determinants

Cardiac output determinants

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Cardiac Output - The Heart's Work Rate

  • Cardiac Output (CO): Volume of blood pumped by the ventricle per minute.
  • Formula: $CO = Heart,Rate,(HR) \times Stroke,Volume,(SV)$.
  • Normal CO is 4-8 L/min.

📌 Mnemonic SV CAP: Stroke Volume is determined by:

  • Contractility
  • Afterload
  • Preload

Cardiac Pressure-Volume Loop with Increased Venous Return

Fick Principle: $CO = \frac{Rate,of,O_2,consumption}{Arterial,O_2,content - Venous,O_2,content}$. This principle is used to calculate CO clinically.

Stroke Volume - Preload, Afterload, Squeeze

Stroke Volume (SV) is the volume of blood pumped from the ventricle per beat. $SV = EDV - ESV$. It is determined by three primary factors:

  • Preload: Ventricular stretch at the end of diastole, approximated by End-Diastolic Volume (EDV).

    • ↑ Preload: IV fluids, exercise, ↑ venous return.
    • ↓ Preload: Nitrates, diuretics, hemorrhage.
    • Cardiac pressure-volume loop with increased venous return
  • Afterload: Resistance the ventricle must overcome to eject blood. Approximated by Mean Arterial Pressure (MAP).

    • ↑ Afterload: Aortic stenosis, systemic hypertension.
    • ↓ Afterload: Vasodilators (e.g., ACE inhibitors), septic shock.
  • Contractility (Squeeze): Intrinsic myocardial contractile force, independent of preload.

    • ↑ Contractility: Catecholamines (dobutamine), Digoxin, ↑Ca²⁺.
    • ↓ Contractility: β-blockers, heart failure, acidosis.

⭐ Increased contractility causes a decrease in End-Systolic Volume (ESV). The heart empties more effectively, increasing the Ejection Fraction ($EF = SV/EDV$).

📌 Mnemonic: Stroke volume is determined by CAP: Contractility, Afterload, Preload.

CO Regulation - Nerves & Hormones

  • Autonomic Nervous System (ANS): The primary, rapid regulator of cardiac output.

  • Hormonal Control: Slower, more sustained effects.

    • Catecholamines (Epi, NE): From adrenal medulla; reinforce sympathetic tone.
    • Thyroid Hormone (T3/T4): Upregulates myocardial β1 receptors, ↑ CO and sensitivity to catecholamines.
    • Glucagon: In β-blocker OD, activates adenylyl cyclase independently of β-receptors → ↑cAMP → ↑HR/inotropy.

⭐ Vagal (parasympathetic) stimulation primarily decreases heart rate (chronotropy) with minimal effect on ventricular contractility (inotropy), as ventricles have sparse vagal innervation.

Autonomic control of heart rate in the medulla

Measurement - Fick's Slick Trick

Fick Principle for Cardiac Output Measurement

  • Based on the principle that oxygen uptake by the lungs equals its consumption by the body.
  • Calculated as: $CO = \frac{\text{O}_2 \text{ consumption}}{\text{Arterial O}_2 \text{ content} - \text{Mixed Venous O}_2 \text{ content}}$
    • Arterial blood is sampled from a systemic artery.
    • Mixed venous blood MUST be sampled from the pulmonary artery.

⭐ The use of mixed venous blood from the pulmonary artery is critical, as it represents the average oxygen saturation after tissue extraction throughout the body.

High‑Yield Points - ⚡ Biggest Takeaways

  • Cardiac Output (CO) is the product of Heart Rate (HR) and Stroke Volume (SV).
  • SV is determined by three key factors: preload, afterload, and contractility (inotropy).
  • Preload is the end-diastolic volume that stretches the ventricle; it's primarily set by venous return.
  • Afterload is the resistance the heart pumps against, like systemic vascular resistance. ↑ Afterload ↓ SV.
  • Contractility is the heart's intrinsic pumping strength. ↑ Contractility ↑ SV.
  • Frank-Starling mechanism: ↑ preload leads to ↑ stroke volume.

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