Cardiac output (CO) reflects the amount of blood pumped by the heart per minute and is a fundamental measure of cardiovascular function. It is influenced by stroke volume (SV) and heart rate (HR) and can be calculated using various physiological formulas.
1. Stroke Volume (SV): The Amount of Blood Ejected Per Beat
SV=EDV−ESVSV = EDV – ESVSV=EDV−ESV
Where:
- EDV (End-Diastolic Volume): The volume of blood in the ventricle before contraction.
- ESV (End-Systolic Volume): The volume of blood remaining in the ventricle after contraction.
🔹 Clinical Relevance:
- Increased SV: Seen in exercise, positive inotropic states (e.g., catecholamines, digoxin).
- Decreased SV: Occurs in heart failure (HF), cardiogenic shock, or increased afterload (hypertension, aortic stenosis).
2. Ejection Fraction (EF): A Measure of Ventricular Contractility
EF=SVEDV×100=EDV−ESVEDV×100EF = \frac{SV}{EDV} \times 100 = \frac{EDV – ESV}{EDV} \times 100EF=EDVSV×100=EDVEDV−ESV×100
- Normal EF: 55-70%
- Reduced EF: Seen in systolic heart failure (HFrEF, EF < 40%).
- Preserved EF: Seen in diastolic heart failure (HFpEF, EF ≥ 50%) due to impaired filling rather than contraction.
3. Cardiac Output (CO): Total Blood Flow per Minute
CO=SV×HRCO = SV \times HRCO=SV×HR
- At Rest: ~5 L/min
- During Exercise: Can increase up to 20-35 L/min in trained athletes.
🔹 Fick Principle (Alternative CO Calculation):CO=O₂ Consumption RateArterial O₂ Content−Venous O₂ ContentCO = \frac{\text{O₂ Consumption Rate}}{\text{Arterial O₂ Content} – \text{Venous O₂ Content}}CO=Arterial O₂ Content−Venous O₂ ContentO₂ Consumption Rate
- Used in critical care settings to measure CO via arterial and venous blood gas analysis.
🔹 Exercise Effects on CO:
- Early Exercise: CO increases due to ↑ SV and ↑ HR.
- Later Exercise: SV plateaus, and CO is maintained by ↑ HR alone.
- Extremely High HR (e.g., Ventricular Tachycardia): Reduces diastolic filling time, lowering SV and CO.
4. Pulse Pressure (PP): Indicator of Arterial Stiffness and Stroke Volume
PP=SBP−DBPPP = SBP – DBPPP=SBP−DBP
- Directly proportional to stroke volume.
- Inversely proportional to arterial compliance.
🔺 Increased PP:
- Aortic regurgitation
- Aortic stiffening (e.g., isolated systolic hypertension in elderly)
- Obstructive sleep apnea (due to ↑ sympathetic tone)
- High-output states (e.g., anemia, hyperthyroidism, exercise – transient effect)
🔻 Decreased PP:
- Aortic stenosis
- Cardiogenic shock
- Cardiac tamponade
- Advanced heart failure
5. Mean Arterial Pressure (MAP): A Key Measure of Organ Perfusion
MAP=CO×TPRMAP = CO \times TPRMAP=CO×TPR MAP=DBP+13PPMAP = DBP + \frac{1}{3}PPMAP=DBP+31PP
- MAP at resting HR: Weighted toward diastolic pressure, as the heart spends more time in diastole.
- MAP < 60 mmHg suggests inadequate perfusion to vital organs (e.g., brain, kidneys).
Clinical Implications:
- Hypertension (↑ MAP): Increases afterload, leading to LV hypertrophy and potential HF.
- Hypotension (↓ MAP): Can indicate shock, sepsis, or severe heart failure, requiring immediate intervention.
- Managing CO and MAP:
- Beta-blockers lower HR, reducing myocardial O₂ demand.
- Vasodilators (ACE inhibitors, ARBs, nitrates) reduce afterload, improving CO in HF patients.
- Fluids & Inotropes (e.g., dobutamine) increase CO in shock states.