Cardiac Output Regulation

Cardiac output (CO) is regulated to maintain adequate blood flow and oxygen delivery to tissues
CO is controlled by the autonomic nervous system, which consists of:
- Sympathetic nervous system (SNS): increases CO
- Parasympathetic nervous system (PNS): decreases CO

Heart rate (HR):
- Increased HR increases CO
- Decreased HR decreases CO
Stroke volume (SV):
- Increased SV increases CO
- Decreased SV decreases CO
Venous return:
- Increased venous return increases CO
- Decreased venous return decreases CO
Contractility:
- Increased contractility increases CO
- Decreased contractility decreases CO

Baroreceptors:
- Located in the walls of large arteries, particularly in the aortic arch and carotid sinus
- Detect changes in blood pressure and send signals to the brain
- Brain responds by increasing or decreasing SNS and PNS activity to regulate CO
Chemoreceptors:
- Located in the carotid and aortic bodies
- Detect changes in oxygen and carbon dioxide levels in the blood
- Send signals to the brain to increase or decrease CO
Volume receptors:
- Located in the atria and ventricles
- Detect changes in blood volume and send signals to the brain
- Brain responds by increasing or decreasing CO

Autonomic nervous system:
- Rapidly adjusts CO in response to changes in blood pressure, oxygen levels, and other factors
- Acts through the SNS and PNS to increase or decrease CO
Hormonal regulation:
- Epinephrine (adrenaline) increases CO
- Norepinephrine increases CO
- Vasopressin (ADH) increases CO

Renin-angiotensin-aldosterone system (RAAS):
- Regulates blood pressure and volume over a longer period
- Activates the RAAS to increase CO and blood pressure
Atrial natriuretic peptide (ANP):
- Released by the atria in response to increased blood volume
- Decreases CO and blood pressure by reducing SNS activity and promoting vasodilation

Cardiac output is regulated to maintain adequate blood flow and oxygen delivery to tissues
Autonomic nervous system (ANS) controls cardiac output, consisting of sympathetic (SNS) and parasympathetic (PNS) nervous systems
SNS increases cardiac output, while PNS decreases it

Heart rate (HR) affects cardiac output:
- Increased HR increases cardiac output
- Decreased HR decreases cardiac output
Stroke volume (SV) affects cardiac output:
- Increased SV increases cardiac output
- Decreased SV decreases cardiac output
Venous return affects cardiac output:
- Increased venous return increases cardiac output
- Decreased venous return decreases cardiac output
Contractility affects cardiac output:
- Increased contractility increases cardiac output
- Decreased contractility decreases cardiac output

Baroreceptors:
- Located in large arteries (aortic arch and carotid sinus)
- Detect changes in blood pressure and send signals to the brain
- Brain responds by increasing or decreasing SNS and PNS activity to regulate cardiac output
Chemoreceptors:
- Located in carotid and aortic bodies
- Detect changes in oxygen and carbon dioxide levels in the blood
- Send signals to the brain to increase or decrease cardiac output
Volume receptors:
- Located in atria and ventricles
- Detect changes in blood volume and send signals to the brain
- Brain responds by increasing or decreasing cardiac output

Autonomic nervous system rapidly adjusts cardiac output in response to changes in:
- Blood pressure
- Oxygen levels
- Other factors
Autonomic nervous system acts through SNS and PNS to increase or decrease cardiac output
Hormonal regulation:
- Epinephrine (adrenaline) increases cardiac output
- Norepinephrine increases cardiac output
- Vasopressin (ADH) increases cardiac output

Renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and volume over a longer period
RAAS activates to increase cardiac output and blood pressure
Atrial natriuretic peptide (ANP) is released by atria in response to increased blood volume
ANP decreases cardiac output and blood pressure by:
- Reducing SNS activity
- Promoting vasodilation