Cardiac output

The core idea

Cardiac output (CO) = heart rate × stroke volume: about 70 × 70 mL, or 5 L/min at rest. Cardiac index is CO divided by body surface area (about 3 L/min/m²). The outputs of the right and left ventricles are equal over time (the left is fractionally larger because bronchial venous blood drains into the pulmonary veins).

Stroke volume and ejection fraction arithmetic

• SV = CO ÷ HR; EF = SV ÷ EDV; ESV = EDV minus SV.
• CO 5.6 L/min at 70 beats/min: SV = 5,600 ÷ 70 = 80 mL. With EDV 145 mL, EF = 80 ÷ 145 = about 55%; with EDV 160 mL, EF = 50%.
• EDV 120 mL and ESV 50 mL: SV 70 mL, EF = 70 ÷ 120 = 58%.

The Frank–Starling law

Within limits, the more the ventricle fills, the more forcefully it contracts, so output is proportional to end-diastolic fibre length (volume). Stretch brings actin and myosin to a better overlap and increases troponin's sensitivity to calcium. The law keeps the two ventricles matched beat by beat.

• In heart failure the curve is flatter and lower: extra filling adds little stroke volume and only raises filling pressures (congestion).
• An inotrope (dobutamine) moves the patient to a higher curve: more stroke volume at the same EDV. Because the ventricle now empties better, end-diastolic volume and wedge pressure fall (24 to 18 mmHg) while stroke volume rises. Inotropes raise myocardial oxygen demand.
• Athletes have a larger, more compliant heart with a higher stroke volume, so the same resting cardiac output is achieved at a lower heart rate.

Law of Laplace

Wall tension = pressure × radius ÷ (2 × wall thickness). A dilated ventricle (larger radius) needs more wall tension to generate the same pressure, so its oxygen demand rises and efficiency falls. Hypertrophy (thicker wall) is the compensation for pressure overload because it lowers wall stress.

Venous return

In a steady state venous return equals cardiac output; the heart can only pump what comes back, so venous return is the main determinant of output.

• Venous return is proportional to mean systemic filling pressure minus right atrial pressure, divided by resistance to venous return. Mean systemic filling pressure (about 7 mmHg) is the pressure in the circulation if the heart stopped.

• Supine hypotension of pregnancy: the gravid uterus (especially with twins) compresses the inferior vena cava, cutting venous return, preload and output; the left lateral position relieves it. In cardiac arrest in late pregnancy, displace the uterus to the left.
• Central line insertion: a deep breath with the hub open lowers intrathoracic pressure below atmospheric and can draw in air. Position the patient head-down (Trendelenburg) so the neck veins are distended above atmospheric pressure; remove lines head-down or flat as well.
• Nitrates (GTN) are venodilators that reduce preload, relieving pulmonary oedema; at higher doses they also lower afterload and dilate coronaries. That makes IV GTN the best choice for intra-operative hypertension in a patient with asthma and angina, where β-blockers are unsafe.

Measuring cardiac output

• Fick principle: CO = oxygen consumption ÷ (arterial O2 content minus mixed venous O2 content). Example: 250 mL/min ÷ (200 − 150 mL/L) = 5 L/min. True mixed venous blood comes from the pulmonary artery.
• Indicator (dye) dilution: a known amount of indocyanine green is injected into a central vein and its concentration is measured over time in arterial blood (a peripheral artery or the aorta). CO = amount injected ÷ area under the concentration curve. Thermodilution (cold saline via a pulmonary artery catheter) uses the same principle. Inulin measures GFR, not cardiac output.

Responses worth reasoning through

• A fall in arterial pressure reduces carotid sinus firing, which raises sympathetic outflow, heart rate and contractility.

Exam trap Preload is end-diastolic volume, not aortic pressure (afterload); mixed venous blood is taken from the pulmonary artery.

Natriuretic peptides and heart failure

• Stretched atria release ANP, ventricles release BNP; both cause natriuresis and vasodilatation and oppose renin–angiotensin–aldosterone. BNP or NT-proBNP diagnoses and monitors heart failure.
• In low-output failure, sympathetic, renin–angiotensin and ADH activation retain salt and water and constrict vessels; long term this remodels the heart, which is why neurohormonal blockers improve survival.

Remember The heart pumps what it receives; Starling matches output to filling.

How FCPS asks about this

• EF with HR 70, CO 5.6 L, EDV 145 mL: SV 80 mL, EF about 55%.
• Dilated heart needs more wall tension: law of Laplace.
• Dobutamine on the Starling curve: higher stroke volume at the same EDV; wedge pressure falls.
• Dizziness supine at 32 weeks with twins: IVC compression cuts venous return.
• Indicator-dilution dye: indocyanine green, sampled from arterial blood.
• Position for central line insertion: head-down to prevent air embolism.
• Venous return from legs while jogging: skeletal muscle pump with venous valves.