Cardiovascular
Blood Circulation
Pulmonary and systemic circuits — the heart as two pumps in series
The cardiovascular system is two circuits driven by a single four-chambered pump. The right heart receives deoxygenated systemic venous blood and propels it through the pulmonary circulation, where CO₂ is offloaded and oxygen acquired. The left heart receives oxygenated pulmonary venous blood and ejects it into the systemic arteries, perfusing every tissue. The arrangement is in series, so right and left cardiac output must match over time. Pressures differ dramatically — pulmonary systolic ~25 mmHg versus systemic ~120 mmHg — reflecting the very different vascular resistances of the two beds. Resting cardiac output is about 5 L/min, climbing to 25 L/min during exercise.
- Resting cardiac output~5 L/min (heart rate × stroke volume)
- Systemic systolic pressure~120 mmHg
- Pulmonary systolic pressure~25 mmHg
- Capillary surface area~600-700 m²
- Total blood volume~5 L (70 kg adult)
- Resting circulation time~1 minute (full circuit)
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Why blood circulation matters
- Cardiology. All cardiac disease — ischemia, valvular, heart failure, arrhythmia — alters circulation in ways that drive symptoms and treatment.
- Critical care. Shock states classify by circulatory derangement: hypovolemic, cardiogenic, distributive, obstructive — each demands different resuscitation.
- Anesthesia. Every anesthetic agent alters preload, afterload, contractility, or rate; managing circulation is core to safe anesthesia.
- Surgery. Massive transfusion protocols, hemodynamic monitoring, and tissue perfusion all rest on circulatory physiology.
- Pulmonology. Right heart catheterization measures pulmonary pressures and is the gold standard for diagnosing pulmonary hypertension.
- Pregnancy. Cardiac output rises 30-50%, plasma volume 50%, and red cell mass less — explaining "physiological anemia of pregnancy."
- Sports medicine. Athletic adaptation to training is largely cardiovascular — eccentric ventricular hypertrophy, increased stroke volume, lower resting heart rate.
Common misconceptions
- "The heart is one pump." It is two pumps in series — right and left can fail independently and present very differently.
- "Cardiac output equals blood pressure." Pressure depends on output and resistance; high BP can coexist with low output (decompensated HF).
- "Veins return blood passively." Skeletal muscle pump, respiratory pump, and venous tone actively drive return; venous failure causes shock.
- "Pulmonary edema means heart failure only." ARDS, neurogenic, and high-altitude pulmonary edema have non-cardiogenic mechanisms.
- "Higher heart rate means better perfusion." Beyond a point, tachycardia shortens filling and ejection time, dropping output.
- "Capillaries pulsate." Pulsatility is dampened in arterioles; capillary flow is largely continuous in healthy circulation.
Frequently asked questions
How do the two circuits work?
Systemic venous blood returns to the right atrium via the superior and inferior venae cavae, flows into the right ventricle, and is ejected through the pulmonary valve into the pulmonary artery. Pulmonary capillaries surround alveoli, where gas exchange occurs. Oxygenated blood returns through pulmonary veins to the left atrium, fills the left ventricle, and is ejected through the aortic valve into the aorta. The same blood volume traverses both circuits per beat — about 70 mL per stroke at rest.
What's cardiac output?
Cardiac output (CO) = stroke volume × heart rate. Stroke volume depends on preload (end-diastolic volume — Frank-Starling), afterload (resistance to ejection), and contractility. Heart rate is set by the sinoatrial node, modulated by autonomic tone. Resting CO of ~5 L/min can rise to 25 L/min during maximal exercise via increased rate (up to ~3-fold) and stroke volume (up to ~2-fold). The cardiac index normalizes CO to body surface area, with normal range 2.5-4.0 L/min/m².
How is blood pressure regulated?
Mean arterial pressure (MAP) ≈ CO × systemic vascular resistance. Short-term regulation is via baroreceptors in the carotid sinus and aortic arch — they sense stretch and modulate sympathetic and parasympathetic tone within seconds. Medium-term involves the renin-angiotensin-aldosterone system. Long-term regulation is renal — kidney pressure-natriuresis sets blood volume to match cardiovascular needs. Most antihypertensives act somewhere along this axis.
Why are pulmonary pressures lower?
The pulmonary circulation is short, low-resistance, and highly distensible. It must accept the entire cardiac output but can do so at low pressure because the alveolar capillary network is enormous and arterioles thin-walled. Lower pressure reduces transudation into alveoli and protects gas exchange. When pulmonary pressures rise (pulmonary hypertension), right ventricular failure follows. The right ventricle is built for low afterload — it tolerates volume overload but fails with sustained pressure overload.
How does venous return work?
Venous return depends on the pressure gradient from peripheral veins to the right atrium. Skeletal muscle pump and one-way venous valves drive flow from extremities. Respiratory pump uses negative intrathoracic pressure during inspiration to enhance venous return. Veins act as capacitance vessels — they hold ~70% of blood volume and can recruit it via sympathetic venoconstriction. Loss of venous tone in distributive shock (sepsis, anaphylaxis) drops venous return and cardiac output despite normal pump function.
What's special about coronary circulation?
The heart receives blood through the right and left coronary arteries from the aortic root. Unlike most beds, coronary perfusion occurs predominantly during diastole, because systolic compression closes intramural vessels. Tachycardia shortens diastole disproportionately, limiting coronary supply just when demand is highest — the basis of demand ischemia. Coronary blood flow is tightly autoregulated to match myocardial oxygen demand; failure of this match in atherosclerotic disease produces angina and infarction.
How does exercise change circulation?
Sympathetic activation increases heart rate and contractility. Skeletal muscle vasodilation (driven by adenosine, nitric oxide, and metabolic byproducts) lowers systemic vascular resistance dramatically. Splanchnic and renal vasoconstriction shunts flow to active muscle. Cardiac output rises 4-5 fold. Stroke volume increases through both higher contractility and increased preload from muscle pump. Trained endurance athletes can reach cardiac output of 35-40 L/min — 7-fold above rest — with much of the gain in stroke volume.