Blood pressure (BP) is a key aspect of the cardiovascular system, which consists of the heart (cardio) and blood vessels (vascular).
The primary factors affecting BP are:
Heart: responsible for generating the pressure through its pumping action.
Blood Vessels: their resistance, particularly the diameter (radius), plays a crucial role in affecting blood flow and pressure.
Cardiac Output (CO): the volume of blood pumped by the heart in one minute; calculated by:
CO = Stroke Volume × Heart Rate
Peripheral Resistance: related to the resistance in blood vessels.
The most important factor in resistance is the radius of blood vessels:
Decreased radius = Vasoconstriction (increases resistance)
Increased radius = Vasodilation (decreases resistance)
Blood Pressure can be expressed as:
BP = CO × Peripheral Resistance
Changes in CO and resistance greatly influence BP:
Increase in heart rate or stroke volume leads to increased CO and thus increased BP.
Increase in resistance (due to vasoconstriction) leads to increased BP.
It's vital to maintain BP:
Low BP can lead to inadequate blood supply to tissues.
High BP can cause damage to blood vessels and organs.
Short-term regulation primarily uses the nervous system, while long-term regulation involves hormonal responses and the urinary system.
The body responds to changes in BP quickly through:
Baroreceptors: pressure sensors located in arteries.
They detect stretch of arterial walls due to BP changes.
Signals from baroreceptors sent to the medulla oblongata to assess BP status.
A high rate of signals indicates high BP; low signals indicate low BP.
Sympathetic Nervous System activation leads to:
Increased heart rate and contractility (increased CO).
Vasoconstriction, increasing peripheral resistance.
Parasympathetic Nervous System activation reduces heart rate and thus lowers BP.
Involves hormonal control and kidney function:
Renin-Angiotensin-Aldosterone System (RAAS):
Kidneys release renin in response to low BP.
Renin converts angiotensinogen (from the liver) into angiotensin I.
Angiotensin I is converted to angiotensin II by Angiotensin Converting Enzyme (ACE) in the lungs.
Angiotensin II acts to:
Stimulate thirst and fluid intake, increasing blood volume.
Cause vasoconstriction, increasing resistance.
Stimulate aldosterone release, promoting sodium and water retention by kidneys.
Stimulate Antidiuretic Hormone (ADH) to promote water reabsorption in kidneys.
Hypertension can lead to adaptations in baroreceptors, making them less sensitive to high BP.
Treatment of hypertension often involves multiple medications to:
Lower heart rate and contractility (reducing CO).
Cause vasodilation to lower peripheral resistance.
Use diuretics to manage blood volume.
Caution is needed—rapidly lowering BP can trigger compensatory mechanisms, raising BP back to abnormal levels.
Management of hypertension is gradual, as it mimics long-term physiological changes.