“The **pulmonary circulation receives the entirety of the cardiac output (CO) from the right ventricle** whilst maintaining low pressures and low resistance… Collectively, such findings indicate that sympathetically mediated pulmonary vasoconstriction could restrain excessive vasodilatation of the compliant pulmonary vasculature when **CO is increased; however, passive flow‐related dynamics are the predominant influence**.” This indicates that pulmonary blood flow mainly follows changes in cardiac output, with autonomic effects acting more to modulate vascular tone and stiffness than to drive flow.

This review notes that sympathetic activation during stress and exercise increases heart rate, contractility, and peripheral vasoconstriction, leading to an increase in cardiac output and blood pressure. It states that **sympathetic neural outflow to the heart and vasculature is a primary mechanism for acute cardiovascular adjustments** to stressors such as exercise and orthostatic challenge. This supports the role of sympathetic activation in acutely elevating cardiac output, which in turn increases pulmonary blood flow because all the cardiac output must pass through the lungs.

With exposure to acute hypoxia (i.e. 0–12 h), cardiac output becomes elevated primarily because of an increase in heart rate, whereas stroke volume is maintained.[5] This initial response is necessary to maintain oxygen delivery in the face of decreased oxygen saturation. In summary, global and regional biventricular function are supported by sympathetic activation that counters RV afterload to ultimately maintain stroke volume. When coupled with increased heart rate, the preserved stroke volume allows for a greater cardiac output in acute hypoxia.[5] Because pulmonary blood flow equals cardiac output in the absence of significant shunt, an increase in cardiac output during acute stress or hypoxia directly increases total pulmonary blood flow.

During exercise, increases in cardiac stroke volume and heart rate raise cardiac output, which coupled with a transient increase in systemic vascular resistance, maintains arterial pressure despite a large decrease in systemic vascular resistance in active muscles. The rise in cardiac output during dynamic exercise is matched by an equivalent increase in pulmonary blood flow, allowing adequate gas exchange across the lungs.

Under a section describing stress responses, the text states that activation of the sympathetic nervous system and adrenal medulla during stress such as exercise, hemorrhage, or emotional stress leads to catecholamine release. It notes: “The overall cardiovascular response [to circulating norepinephrine] is increased cardiac output and systemic vascular resistance, which results in an elevation in arterial blood pressure.” For epinephrine at low-to-moderate concentrations it states: “The overall cardiovascular response … is increased cardiac output and a redistribution of the cardiac output to muscular and hepatic circulations, with only a small change in mean arterial pressure.”

The study examined cardiovascular reactions to acute psychological stress in adolescents. Higher heart rate and cardiac output reactivity were observed during the stress tasks compared with baseline.[6] The authors note that 'higher heart rate and cardiac output reactivity' characterize the acute stress response and are mediated by sympathetic activation. These findings are consistent with a broader literature showing that acute psychological stress typically elicits increased cardiac output rather than a reduction.[6]

During mental stress mean PAP (± SEM) increased by 9.4 ± 2.1 mm Hg (P < 0.005). Pulmonary vascular resistance increased by 149 ± 25 dyne s cm−5 (P < 0.001). Stroke volume decreased by 6.6 ± 2.2 ml (P < 0.03).[2] The data show that moderate mental stress increases right heart afterload in patients with severe pulmonary hypertension owing to elevation of PVR.[2] In this specific population, stress did not increase cardiac output; instead, the elevated pulmonary vascular resistance and pulmonary artery pressure opposed right‑ventricular ejection, so pulmonary blood flow did not rise despite the stress response.

“As described above, the pulmonary (right heart) and system (left heart) circulations are arranged in a series. Thus, **cardiac output increases in each at the same rate; hence an increased systemic need for a greater cardiac output will automatically lead to a greater flow of blood through the lungs** (a greater potential for O2 delivery).” This describes that any increase in overall cardiac output directly causes increased pulmonary blood flow because the two circulations are in series.

“The overall effect of **sympathetic activation is to increase cardiac output, systemic vascular resistance (both arteries and veins), and arterial blood pressure.** Enhanced sympathetic activity is important during exercise, emotional stress, and during hemorrhagic shock.” Sympathetic activation increases heart rate and contractility, which increases cardiac output: “activation of sympathetic efferent nerves to the heart increases heart rate (positive chronotropy), contractility (positive inotropy)…”. This provides the mechanism by which acute stress (via sympathetic activation) increases cardiac output.

During exercise, the gas exchange requirements of the lung increase due to increased oxygen consumption and increased carbon dioxide production. There are also cardiac changes; an increase in heart rate and stroke volume causes an increase in cardiac output. This results in an increase in pulmonary circulation. Blood flow is redistributed, with more blood being directed to the middle and upper zones via the recruitment of more pulmonary capillaries.

Cardiac output is the term that describes the amount of blood your heart pumps each minute. During exercise, your body may need three or four times your normal cardiac output, because your muscles need more oxygen when you exert yourself. Generally speaking, your heart beats both faster and stronger to increase cardiac output during exercise. Since the pulmonary and systemic circulations are connected in series, this rise in cardiac output is accompanied by an equivalent increase in blood flow through the lungs.

In the section on exercise, the text explains that in healthy young individuals, “HR may increase to 150 bpm during exercise. SV can also increase from 70 to approximately 130 mL/beat. This increases CO to as much as 19.5 L/min, compared to 5 L/min at rest.” It further notes that during sympathetic activation, catecholamines increase heart rate and contractility, enhancing cardiac output and thereby systemic and pulmonary blood flow.

This experimental study reports: “The results of this study indicate that at control vascular tone the catecholamines norepinephrine and epinephrine increase pulmonary vascular resistance and decrease pulmonary vascular compliance through alpha 1- and alpha 2-receptor-mediated stimulation…”. It continues: “When vascular tone was elevated, the effect of norepinephrine and epinephrine on pulmonary vascular resistance was not present, which may be due to the appearance of a more pronounced vasodilatory beta 2-receptor system and an attenuation of the alpha-mediated vasoconstrictor responses.” The authors conclude that altered adrenergic responses may affect pulmonary capillary pressure, an important determinant of lung fluid balance.

Using a feline model with controlled pulmonary blood flow, the authors state: “We investigated the effects of catecholamines and sympathetic nerve stimulation in the feline pulmonary vascular bed under conditions of controlled pulmonary blood flow.” They report that “Norepinephrine and nerve stimulation caused dose- and stimulus frequency-dependent increases in pulmonary vascular resistance.” However, “when pulmonary vascular tone was enhanced and alpha receptors blocked, norepinephrine and nerve stimulation caused dose- and frequency-dependent decreases in pulmonary vascular resistance.” The study demonstrates that catecholamines primarily alter pulmonary vascular resistance and tone, while blood flow was experimentally held constant.

This classic study on dogs examined pulmonary arterial pressure responses to acute hypoxia. The abstract notes that the pulmonary pressor response persisted after adrenalectomy and cardiac denervation but was reduced by alpha-adrenergic blockade. The authors state that catecholamines contribute to the pulmonary arterial pressure rise but also emphasize that changes in pulmonary arterial pressure occurred “without significant changes in cardiac output,” indicating that pulmonary vascular constriction, not increased flow, was the main determinant of the pressure response in this model of acute stress (hypoxia).

During exercise, blood flow increases in proportion to the metabolic needs of the muscles. Cardiac output rises due to increases in both heart rate and stroke volume, and this augmented output must pass through the pulmonary circulation before reaching the systemic arterial tree. Because right and left heart outputs are normally matched, any acute increase in cardiac output during exercise necessarily results in a corresponding increase in pulmonary blood flow.

In this physiology video, the presenter explains: “If we increase [venous return/preload]… that will increase our stroke volume, thus **increasing our cardiac output.**” Later, he adds, “If you remember, **sympathetic stimulation prepares your body for fight or flight… these guys are going to increase cardiac output.** They’re going to increase heart activity.” This illustrates how extrinsic (sympathetic) control during stress increases cardiac output by boosting heart rate and contractility, which would proportionally raise pulmonary blood flow since it equals cardiac output.

In standard cardiovascular physiology, the **pulmonary circulation is arranged in series with the systemic circulation**, so in steady state, pulmonary blood flow is effectively equal to cardiac output from the right ventricle. During acute sympathetic stress (e.g., exercise, fight-or-flight), pulmonary blood flow primarily increases because cardiac output rises (via increased heart rate and contractility and often increased venous return). Autonomic effects on pulmonary vascular tone modulate pressures and resistance, but the dominant determinant of increased flow is the elevated cardiac output.