Cardiac output explanations with flowcharts and diagrams

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Cardiac Output - Complete Guide with Diagrams

1. Definition and Core Formula

Cardiac output (CO) is the total volume of blood ejected by the left ventricle per minute.

CO = Stroke Volume (SV) × Heart Rate (HR)

Parameter	Definition	Normal Value
Cardiac Output	Volume ejected per minute	~5,000 mL/min (5 L/min)
Stroke Volume	Volume ejected per single beat	~70 mL
Heart Rate	Beats per minute	~72 bpm
Ejection Fraction	SV ÷ End-diastolic volume	~50-65%

Sample calculation (from Costanzo Physiology):

EDV = 140 mL, ESV = 70 mL, HR = 75 bpm
SV = EDV - ESV = 140 - 70 = 70 mL
CO = 70 mL × 75 bpm = 5,250 mL/min
EF = 70/140 = 0.50 (50%)

2. Master Flowchart of Cardiac Output Regulation

                    CARDIAC OUTPUT
                   CO = SV × HR
                  /              \
         STROKE VOLUME          HEART RATE
        /      |      \         /        \
   Preload  Afterload Contractility  Sympathetic  Parasympathetic
      ↑         ↓         ↑           ↑ HR           ↓ HR
   (EDV)    (SVR/BP)  (Inotropy)   (↑ inotropy)   (vagal tone)

3. Cardiac Index

The cardiac index normalizes CO for body surface area:

Cardiac Index = CO ÷ Body Surface Area (BSA)

Normal adult: ~3.0 L/min/m² (for 70 kg, 1.7 m² BSA)
Peaks at age 10: >4 L/min/m²
Declines to ~2.4 L/min/m² by age 80

Cardiac index vs. age - declines from peak at age ~10 to ~2.4 L/min/m² at age 80

Fig. 20.1 - Guyton & Hall: Cardiac index across the lifespan

4. The Three Determinants of Stroke Volume

A. Preload

Defined as the ventricular load at end-diastole, before contraction begins
Clinically estimated by: PCWP (pulmonary capillary wedge pressure), CVP, or echocardiographic EDV
Greater preload → greater stretch → greater SV (Frank-Starling law)

B. Afterload

Defined as the systolic load after contraction begins
Clinically approximated by systolic blood pressure (when aortic stenosis is absent)
Governed by Laplace's Law:

Wall Stress (σ) = P × R / (2 × h)

P = pressure, R = radius, h = wall thickness

Laplace's Law diagram showing LV wall stress, radius, wall thickness, and comparison of normal LV vs aortic stenosis pressures

Fig. 13.3 - Miller's Anesthesia: Laplace's Law and LV wall stress. In aortic stenosis, compensatory LV hypertrophy (↑h) normalizes wall stress despite higher pressure.

C. Contractility (Inotropy)

The intrinsic ability of the heart to generate force at a given end-diastolic volume
Increased by: sympathetic stimulation, catecholamines, milrinone, digoxin, exercise, ↑Ca²⁺
Decreased by: heart failure, ↓pH, hypothermia, beta-blockers, myocardial ischemia

5. Frank-Starling Mechanism

The Frank-Starling law states: the greater the end-diastolic volume (stretch), the greater the stroke volume and cardiac output - up to an optimal sarcomere length.

Molecular basis: Longer sarcomere length (2.0-2.2 μm) → optimal actin-myosin overlap → increased cross-bridge cycling and increased Ca²⁺ sensitivity of myofilaments.

Frank-Starling curve showing stroke volume (mL) rising as ventricular end-diastolic volume increases, with sarcomere diagrams showing normal vs. optimal overlap

Fig. 13.4 - Miller's Anesthesia: Frank-Starling curve. As EDV rises, stroke volume increases. Insets show sarcomere length and actin-myosin overlap at different points.

Family of Frank-Starling Curves

Contractility shifts the entire curve up or down:

Fig. 13.5 - Miller's Anesthesia: A family of Frank-Starling curves. Leftward/upward shift = enhanced inotropy (exercise, catecholamines). Rightward/downward shift = impaired inotropy (heart failure, myocardial depression).

6. Ventricular Function Curves (Starling Curves)

These show stroke work output or ventricular volume output vs. atrial filling pressure:

Left and right ventricular stroke work vs. mean atrial pressure - both curves plateau at higher filling pressures

Fig. 9.12 - Guyton & Hall: Stroke work output curves for LV and RV. As atrial pressure rises, stroke work increases until the ventricle's limit.

Ventricular volume output (L/min) vs. atrial pressure - right ventricle responds at lower pressures than left

Fig. 9.13 - Guyton & Hall: Volume output curves. The RV (blue) reaches max output at much lower atrial pressures than the LV (red), reflecting the low-pressure pulmonary circuit.

7. Pressure-Volume Loop

The PV loop is the gold-standard tool to assess ventricular contractility:

Pressure-volume loop showing 4 phases: isovolumetric contraction (a→b), ejection (b→c), isovolumetric relaxation, and filling (d→a); internal work (red) and external work (pink) labeled

Fig. 13.6 - Miller's Anesthesia: Pressure-Volume loop. Point a = start of isovolumetric contraction; b = aortic valve opens (ejection); c = end-systole; d = mitral valve opens (filling). The width of the loop = stroke volume. The slope of the end-systolic PV relationship (Es) = contractility index.

Reading the loop:

Wider loop (more horizontal) = greater SV = higher CO
Steeper Es slope = better contractility
In heart failure: narrower loop, shifted right, flatter Es

8. Autonomic Control of CO

Cardiac sympathetic and parasympathetic innervation - sympathetic chain bilaterally, vagus nerves, SA node and AV node labeled

Fig. 9.14 - Guyton & Hall: Cardiac autonomic innervation. Sympathetic nerves (yellow) supply SA node, AV node, and myocardium bilaterally. Vagus carries parasympathetic fibers.

Stimulus	HR Effect	Contractility Effect	Net CO Change
Sympathetic activation	↑ (chronotropy)	↑ (inotropy)	↑↑ (up to 3x)
Parasympathetic (vagal)	↓↓ (can arrest heart)	↓ (mild)	↓
Normal resting tone	Sympathetic maintains CO ~30% above zero

Strong sympathetic stimulation can raise HR from 70 to 180-250 bpm and can double contractility, increasing max CO 2- to 3-fold beyond Frank-Starling alone.

9. Measuring Cardiac Output - The Fick Principle

The Fick principle states that O₂ consumption by the body = O₂ leaving lungs - O₂ returning to lungs:

         O₂ Consumption (mL/min)
CO = ─────────────────────────────────────────────────
     [O₂]pulmonary vein - [O₂]pulmonary artery

Sample (Costanzo Physiology):

O₂ consumption = 250 mL/min
Arterial O₂ content = 0.20 mL O₂/mL blood
Pulmonary arterial O₂ content = 0.15 mL O₂/mL blood

CO = 250 / (0.20 - 0.15) = 250 / 0.05 = 5,000 mL/min

Key assumption: In steady state, right heart CO = left heart CO.

Other CO measurement methods: thermodilution (Swan-Ganz catheter), echocardiography (outflow tract VTI), dye dilution.

10. Summary: Factors That Change Cardiac Output

Factor	Change	Effect on CO
Venous return (preload)	↑	↑ CO (Frank-Starling)
Heart rate	↑ (moderate)	↑ CO
Heart rate	↑↑ (extreme, >180)	↓ CO (↓ diastolic filling)
Contractility	↑	↑ CO (curve shifts up)
Afterload (SVR/BP)	↑↑	↓ SV, ↓ CO
Sympathetic activation	↑	↑ CO
Parasympathetic/vagal	↑	↓ CO
Heart failure	-	↓ CO, curve shifts down
Exercise	-	↑ CO (up to 5x in athletes)
Aortic stenosis	-	↑ afterload, ↓ CO

Sources: Guyton and Hall Textbook of Medical Physiology, Costanzo Physiology 7th Edition, Miller's Anesthesia 10th Edition

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