Cardiac Output & Stroke Volume Comprehensive Notes

Definition & Core Equation

• Cardiac Output (CO)
  • Volume of blood ejected per minute by the left ventricle.
  • Units: litres · min⁻¹.
  • Fundamental equation: CO = HR \times SV
  • HR = Heart Rate (beats · min⁻¹)
  • SV = Stroke Volume (mL · beat⁻¹)

Normal Reference Values & Perspective

• Resting CO in an average 6-ft adult male ≈ 5 L · min⁻¹.
• Entire blood volume (~ 5 L) therefore recirculates once each minute at rest.
• In fight-or-flight (sympathetic activation) both HR and SV rise → CO increases markedly to meet muscular O₂ demand.

Stroke Volume & Ventricular Volume Terminology

• Stroke Volume (SV): blood ejected per beat.
  • Calculated by: SV = EDV - ESV
• End-Diastolic Volume (EDV)
  • Volume inside the ventricle after filling (end of diastole).
• End-Systolic Volume (ESV)
  • Volume remaining after contraction/ejection (end of systole).

Example (graph reference)

• EDV = 130 mL, ESV = 70 mL ⇒ SV = 60 mL.

Determinants of Cardiac Output

• Direct from CO = HR \times SV →
  • ↑HR or ↑SV → ↑CO
  • ↓HR or ↓SV → ↓CO

1 | Heart Rate (quick review)

• Extrinsic control via autonomic nerves & hormones
  • Sympathetic (↑ NE, Epi) → ↑HR
  • Parasympathetic (vagus, ACh) → ↓HR
• HR changes also alter filling time, indirectly influencing SV (see Preload).

2 | Stroke Volume (focus of video)

Three constantly active modifiers:

1. Contractility (extrinsic)
2. Preload (EDV-dependent; intrinsic – Frank-Starling)
3. Afterload (arterial resistance)

Contractility

• Definition: change in force of contraction at a given EDV.
• Extrinsic (neural/hormonal) influence; primary drivers:
  • Norepinephrine (NE) – sympathetic neurotransmitter
  • Epinephrine (Epi) – adrenal hormone
• Mechanistic note: ↑ Ca²⁺ influx → more cross-bridge cycling → stronger twitch.
• Graphically: upward shift of SV vs EDV curve when sympathetic tone rises.

Clinical/Predictive Points

• Positive inotropes (e.g., digitalis) mimic ↑contractility.
• β-blockers ↓contractility, useful in HTN or arrhythmia management.

Preload & the Frank-Starling Law

• Preload = end-diastolic pressure (tension) on ventricular wall caused by EDV.
• Frank-Starling Principle: \uparrow EDV \Rightarrow \uparrow stretch \Rightarrow optimal sarcomere length \Rightarrow \uparrow cross-bridges \Rightarrow \uparrow force \Rightarrow \uparrow SV
  • Intrinsic; does not require neural/hormonal input.
• Sarcomere length-tension relationship:
  • More blood → longer sarcomeres (still on ascending limb for healthy heart) → more myosin heads bind actin.
  • Too little blood → overlapping thin filaments block binding sites → weaker contraction.

Determinants of EDV / Preload

1. Filling Time
   • Longer diastole → ↑EDV; shorter diastole (high HR) → ↓EDV.
2. Atrial Pressure Gradient (Atrial P – Ventricular P)
   • Governed mainly by venous return (VR).
   • Poiseuille perspective: Q \propto \Delta P.

Interplay During Fight-or-Flight

• Sympathetic ↑HR → ↓filling time, which would ↓EDV.
• Simultaneous sympathetic effects on veins (venoconstriction) → ↑VR, offsetting lost time.
• Net: Starling effect maintained, contractility greatly ↑ → overall ↑SV despite tachycardia.

Afterload

• Defined as the arterial pressure the ventricle must exceed to open semilunar valves and eject blood.
  • Practically: aortic pressure (left ventricle) or pulmonary trunk pressure (right).
• Relationship: \uparrow Afterload \Rightarrow \downarrow SV
  • More time spent in isovolumetric contraction, less time/energy left for ejection.

Physiological & Pathological Contexts

• Healthy heart
  • Modest BP rises (normal range) → minimal SV change.
• Exercise / Hypertension
  • Higher afterload begins to curb SV.
• Heart Failure
  • Weakened myocardium: even normal afterload markedly depresses SV; curve becomes very steep.
  • Clinical rationale for afterload-reducing drugs (e.g., ACE inhibitors).

Integrative Graph Logic (EDV vs SV with Contractility)

• Holding EDV constant:
  • ↑Sympathetic → upward shift → ↑SV (higher contractility)
  • ↓Sympathetic → downward shift → ↓SV
• Holding Sympathetic tone constant:
  • ↑EDV → rightward move along curve → ↑SV (Starling)
  • ↓EDV → leftward → ↓SV

Key Distinction Heuristic

• Changes in EDV → change sarcomere length → modify SV but leave ESV similar.
• Changes in Contractility → change ESV (more/less blood left) without altering EDV.

Real-World & Ethical/Clinical Implications

• Exercise Prescription
  • Understanding preload/afterload assists safe training in hypertensive or CHF patients.
• Drug Development
  • Targeting β-receptors (contractility) vs ACE pathway (afterload) vs venous tone (preload) offers tailored therapy.
• Emergency Care
  • CO estimation critical in shock management; manipulating VR (fluids), contractility (inotropes), or afterload (vasopressors) saves lives.

Numerical & Formula Summary

• CO_{rest} \approx 5\,L\,min^{-1} (avg male).
• Example calc: 70\,beats\,min^{-1} \times 70\,mL\,beat^{-1} = 4.9\,L\,min^{-1}.
• SV = EDV (130\,mL) - ESV (70\,mL) = 60\,mL.
• Flow (Poiseuille): Q \propto \Delta P / R → shows why ↑atrial-ventricular ΔP accelerates filling.

Preload vs Afterload Quick-Look

• Preload
  • Source: blood inside ventricle (EDV).
  • Acts before contraction; stretches muscle.
  • “Load the heart must handle at start of beat.”
• Afterload
  • Source: pressure outside ventricle (aorta/pulmonary trunk).
  • Acts after contraction begins; opposes ejection.
  • “Load the heart must overcome during the beat.”

Key Take-Home Messages

• CO is a simple product of HR and SV, yet under multilayered regulation.
• Contractility (extrinsic), Preload (intrinsic), and Afterload (vascular) interact continuously.
• Starling mechanism allows the heart to self-adjust to incoming volume.
• High afterload or impaired contractility (heart failure) dramatically compromise SV and CO.
• Understanding these dynamics underpins clinical interventions and optimises athletic performance.