Blood Pressure Measurement Techniques

Study Notes

Diastolic pressure is the second number in blood pressure readings, indicating pressure after heart contraction and before the next contraction (80 mmHg example).
Measurement methods include:
- Manual: Using an aneroid or mercury sphygmomanometer.
- Digital: Automated monitors using oscillometric sphygmomanometers, which may be inaccurate in 5-15% of patients.
- Invasive: Direct measurement of arterial pressure through cannulation of arteries (typically radial), using non-compressible tubing with heparinized saline.

Regulation mechanisms include:
- Short-Term (Neurally Mediated Baroreceptor Mechanism): Rapid adjustments by the autonomic nervous system (ANS).
- Long-Term (Hormonal Regulation): Involves the renin-angiotensin-aldosterone system (RAAS).

Baroreceptors in the aortic arch and carotid sinus detect changes in blood pressure via stretch receptors.
Increased arterial pressure triggers negative feedback to the ANS, decreasing heart rate and contractility, leading to lowered blood pressure.
Decreased arterial pressure causes sympathetic stimulation, increasing heart rate and contractility to raise blood pressure.
The baroreceptor reflex offers minute-to-minute regulation of blood pressure.

Decrease in Arterial Pressure:
- Decreased stretch on carotid sinus walls reduces signals sent to the CNS via Hering's nerve (a branch of cranial nerve IX).
- If mean arterial pressure drops below 100 mmHg:
  - Decreased parasympathetic outflow and increased sympathetic outflow raise blood pressure by:
    - Increasing heart rate (decreased vagal tone).
    - Enhancing contractility and stroke volume.
    - Promoting vasoconstriction of arterioles and veins.
    - Increasing total peripheral resistance (TPR) and venous return, increasing cardiac output through the Frank–Starling mechanism.
Example: Valsalva maneuver tests baroreceptor function; a significant heart rate increase indicates intact reflex mechanism.

Key physiological mechanisms include:
- Renin-Angiotensin-Aldosterone System (RAAS): Controls blood pressure by regulating fluid balance.
- Vasopressin (ADH): Promotes water retention.
- Atrial Natriuretic Peptide (ANP): Promotes sodium excretion.

Renin is released from juxtaglomerular cells in response to:
- Sympathetic stimulation.
- Reduced sodium delivery to the distal convoluted tubule.
- Decreased renal blood flow.
Renin converts angiotensinogen (from the liver) to angiotensin I, which converts to angiotensin II (vasoconstrictor) via ACE.
Angiotensin II promotes sodium reabsorption and aldosterone secretion, leading to water retention and increased blood volume and pressure.
ACE inhibitors and angiotensin receptor blockers are used to lower blood pressure.

Hypertension is a sustained increase in blood pressure and can be primary (unknown cause) or secondary to conditions like chronic renal disease.
It causes vascular damage, leading to atherosclerosis, thromboembolism (risk of MI or stroke), and aneurysms, while also increasing the heart's afterload.