Arterial Blood Pressure (ABP) Regulation

Arterial Blood Pressure (ABP) Regulation Objectives

• Define arterial blood pressure
• Identify normal arterial blood pressure values in different physiological conditions
• Construct mind map to outline different mechanisms that regulate ABP
• Explain the roles of arterial baroreceptors and peripheral chemoreceptors in the regulation of ABP
• Explain rapid/short-term regulation mechanisms for ABP
• Explain intermediate mechanisms that regulate ABP
• Explain long term regulation/slow mechanisms that regulate ABP
• Recognize the cooperation of different body systems to regulate ABP

Vital Signs and Arterial Blood Pressure (ABP)

• Arterial Blood Pressure (ABP) is a vital sign
• Other vital signs include:
  • Heart Rate (HR)
  • Respiratory Rate (RR)
  • Temperature (TEMP)
  • Capillary Refill Time
  • O2 Saturation
  • Arterial Blood Gas (ABG)

Arterial Blood Pressure Definition

• ABP is the lateral pressure exerted by the column of blood on the wall of the arterial system
• Types of arterial blood pressure:
  • Systemic Blood Pressure
  • Pulmonary Blood Pressure

Systolic vs Diastolic Blood Pressure

• Systolic Blood Pressure: the maximal pressure exerted by the column of blood on the wall of the arterial system during systole
• Diastolic Blood Pressure: the minimal pressure exerted by the column of blood on the wall of the arterial system during diastole

Pulse Pressure and Mean ABP Equations

• Pulse Pressure = SBP - DBP
• Mean ABP = DBP + (1/3)PP

Short Term vs Long Term ABP Regulation

• Short Term:
  • Rapid Onset (nervous mechanism)
  • Short Duration (least efficient)
  • Affects vascular tone and capacity
• Long Term:
  • Slow Onset (hormonal mechanism)
  • Long Duration (highly efficient)
  • Affects blood volume

ABP Regulation Timeframes

• Short term regulation:
  • Rapid onset, within seconds
  • Short duration, lasts for a few minutes to a few hours
  • Neuronal mechanism
  • Modulates vascular tone and capacity
• Intermediate term regulation:
  • Starts within a few minutes
  • Lasts for a few hours to days
  • Involves neuronal and hormonal mechanisms
  • Regulates vascular tone, vascular capacity, and blood volume
• Long term regulation:
  • Starts within a few hours
  • Lasts until full correction
  • Hormonal mechanisms
  • Modulates blood volume

Short Term Regulation of ABP

• Mechanisms include:
  • Peripheral arterial baroreflex
  • Peripheral arterial chemoreflex
  • Central Nervous System (CNS) ischemic response
  • Abdominal compression reflex

Intermediate Term Regulation of ABP

• Mechanisms include:
  • Stress relaxation response
  • Capillary fluid shift phenomena
  • Atrial volume (Gauer-Henry) reflex
  • Renin-angiotensin II system

Long Term Regulation of ABP

• Mechanisms include:
  • Pressure diuresis
  • Renin-angiotensin II-aldosterone system

Peripheral Arterial Baroreflex Mechanism

• Stimulus: ABP changes
• Receptor: Aortic and carotid baroreceptors
• Afferent Nerve: Herring nerves
• Center: Cardiovascular center [(SA2) (VCC, CIC, and VDC)]
• Efferent Nerve: Cardiac SNS and cardiac vagal nerve
• Effector Organ: Heart
• Response: Change in HR and modulation of ABP

Increase in ABP

• Leads to activation of aortic and carotid baroreceptors
• Signals sent to Nucleus Tractus Solitarius (NTS) through herring nerves
• NTS activates CIC and VDC, while inhibiting VCC
• Activated CIC sends inhibitory signals through cardiac vagal nerve to Sinoatrial Node (SAN), decreasing HR
• CIC sends inhibitory signals to VCC, leading to Generalized Vasodilation (VD) and reduction of ABP
• Baroreceptor activation inhibits catecholamine secretion, antidiuretic hormone secretion, and the respiratory center
• Restores ABP homeostasis
• The reverse occurs if Artery Blood Pressure (APB) is reduced

Peripheral Arterial Chemoreflex

• Low O2, high CO2, and excess H activate aortic and carotid chemoreceptors
• Signals sent to NTS through herring nerves
• NTS inhibits CIC and VDC, while activating VCC
• Activated VCC sends excitatory signals to heart and blood vessels through Sympathetic Adrenal Medullary (SAM), increasing HR & ABP

CNS Ischemic Response

• Hypotension (MABP below 50 mmHg) leads to CNS ischemia, hypoxia, and high Partial pressure of carbon dioxide (PCO2)
• Stimulates VCC, increasing ABP
• Decreases HR reflexively through Mary's reflex
• Results in the Cushing reflex/reaction

Abdominal Compression Reflex

• Activation of aortic and carotid baro & chemoreceptors
• Stimulates medullary reticular formation
• Sends excitatory signal to somatic nerve that supplies abdominal muscle
• Leads to increased intra-abdominal pressure, increasing venous return
• Increases cardiac output and ABP

Stress Relaxation Mechanism

• Corrects ABP by adjusting vascular capacity in response to changes in blood volume
• If ABP is increased due to volume overload:
  • Stretching the vascular wall occurs
  • Initial increase in the tension in the wall occurs
  • Within a few minutes to hours, the wall tension gradually decreases due to plasticity
  • ABP returns toward normal

Capillary Fluid Shift Phenomena

• Corrects ABP through regulation of blood volume
• Occurs through shifting of fluid between plasma and interstitial fluid.
• If ABP is increased due to volume overload:
  • Capillary hydrostatic pressure increases
  • Filtration force increases across the capillary membrane
  • Plasma volume decreases
  • ABP returns toward normal

Atrial Volume (Gauer-Henry) Reflex

• Corrects ABP by adjusting the rate of salt and water excretion through the kidney
• Increased Blood Volume:
  • Stimulates volume receptors in the Rt atrium, big veins, and pulmonary artery
  • Leads to
    • Dilation of afferent arteriole
    • Increase glomerular filtration rate(GFR)
    • Increased urine output
    • Increased salt and water excretion
    • Reduced blood volume and ABP toward normal
• Increased Blood Volume:
  • Stimulates volume receptors in the Rt atrium, big veins, and pulmonary artery. Leads to:
    • Inhibition of Antidiuretic Hormone (ADH) release
    • Increased salt and water excretion
    • Reduced blood volume and ABP toward normal
• Increased Blood Volume:
  • Stretching of Rt atrium
    • Triggers Rt atrium release of atrial natriuretic peptide
    • Increased salt and water excretion
    • Reduced blood volume and ABP toward normal

Renin-Angiotensin II System

• Hypotension reduces renal blood flow, causing renal ischemia
• Renal ischemia stimulates renin secretion from Juxtaglomerular cells (JGC)
• Renin converts angiotensinogen to angiotensin I
• In pulmonary circulation, angiotensin I is converted to angiotensin II via Angiotensin-converting enzyme (ACE)
• Angiotensin II effects include:
• Strong arteriolar constriction, increasing total peripheral resistance, increasing ABP
• Mild venoconstriction, increasing Venous Return (VR), increasing Cardiac Output(CO), increasing ABP
• Increased release of noradrenaline from sympathetic postganglionic nerve endings
• Increased antidiuretic hormone (ADH)
• Increased Na and water reabsorption by renal tubule

Renin-Angiotensin II-Aldosterone System

• Hypotension reduces renal blood flow, causing renal ischemia
• Renal ischemia stimulates renin secretion from JGC
• Renin converts angiotensinogen to angiotensin I
• In pulmonary circulation, angiotensin I is converted to angiotensin II via ACE
• Angiotensin II has physiological effects
• Increased aldosterone from zona glomerulosa of adrenal cortex
• Increased Na and water reabsorption by renal tubule

Pressure Diuresis

• Increase in mean ABP
• Increase in GFR
• Increase in urine output
• Increase in Na and water excretion