Blood Pressure Physiology


Blood Pressure Physiology, BP Mechanism, Regulation of Circulation, Blood Flow, Vascular Flow

  • Physiology
  • General
  1. Blood Pressure follows a pressure gradient decreasing as blood enters smaller and smaller vessels (allows for forward flow)
    1. Mean systolic Blood Pressure drops from 100 mmHg in aorta to <80 in arterioles, <35 in capillaries, <10 in venules
      1. Forward flow is also maintained by venous valves and Muscle Contractions
    2. Mean Blood Pressure is lower in the right circulation (16 mmHg pulmonary artery, 7 mmHg right atrium)
      1. Pulmonary artery pressures are lower in the superior lung fields than inferior lung fields due to gravity
    3. Overall Blood Flow
      1. Blood Flow increases with the increasing difference between the pressures at start and ends of vascular circuit
      2. Blood Flow is impacted primarily by Cardiac Output and Peripheral Vascular Resistance
      3. Blood Flow is impacted by normal secondary factors
        1. Lung inspiration (and negative chest pressure) increases venous return
        2. Skeletal Muscle Contraction
          1. Isometric Exercise (constant Muscle length) increases Vasoconstriction and Blood Pressure
          2. Isotonic Exercise (shortening Muscle length) decreases Vasoconstriction and Blood Pressure
        3. Venous pooling (e.g. prolonged standing)
      4. Blood Flow is impacted by chronic disease states
        1. Atherosclerosis with vessel narrowing
        2. Angiogenesis (prolonged tissue Hypoxia such as vascular disease)
        3. Blood viscosity (increased in Polycythemia Vera)
        4. Edematous States (Blood Volume lost to interstitial fluid, e.g Nephrotic Syndrome)
    4. Images
      1. cv_Circuit.jpg
  2. Blood Pressure is maintained by a combination of Peripheral Vascular Resistance and Cardiac Output
    1. Peripheral Vascular Resistance (vascular tone and Vasoconstriction, Afterload)
      1. Diastolic Blood Pressure reflects vascular tone
      2. Vasoconstriction (increased by ADH, Renin/Angiotensin, Aldosterone, Sympathetic Agonists)
      3. Also increased with stiff, non-compliant vessels (aging) and increased blood viscosity
    2. Cardiac Output
      1. Systolic Blood Pressure reflects Cardiac Output
      2. Cardiac Output = (Heart Rate) x (Stroke Volume)
        1. Heart Rate is suppressed at baseline by the Parasympathetic System (Vagus Nerve, vagal tone)
        2. Stroke Volume is dependent on cardiac contractility
      3. Blood Volume (5-6 L in adults, increased by ADH, Aldosterone)
        1. See Sodium and Water Homeostasis
        2. Venous return (Preload) is directly correlated with Stroke Volume (to a maximum)
      4. Sympathetic Nervous System stimulation
        1. Increases Heart Rate, contractility, Vasoconstriction via Epinephrine, Norepinephrine
        2. Stimulates the Renin-Angiotensin System and Aldosterone release
    3. Images
      1. BloodPressureRegulation.jpg
      2. reninAngiotensin.jpg
  1. Blood Carbon Dioxide and pH
    1. Hypercarbia and acidosis stimulate Brainstem with resulting increased sympathetic activity
  2. Serum Osmolality
    1. Increased osmolality and Hypernatremia act at Hypothalamus to increase ADH release
    2. Increases Sensation of thirst (Hypothalamus mediated)
    3. Increased Serum Osmolality also acts at renal tubules to reabsorb water
  3. Heart detection of Blood Volume
    1. Stroke Volume
      1. Cardiac contractility increases with Stroke Volume until a maximum (Starling's Law)
    2. Atrial Natriuretic Factor (ANF)
      1. Atrial wall stretches with increased Blood Volumes and releases ANF
      2. ANF acts to decrease fluid volume
        1. Increases renal tubular Sodium (and water) excretion
        2. Increases GFR (afferent arteriole vasodilation via relaxed Mesangial Cells)
        3. Suppresses plasma renin and Aldosterone release
  4. Peripheral Vascular Resistance
    1. Vasoconstriction increases with ADH, Renin/Angiotensin, Aldosterone, Sympathetic Agonists)
    2. Blood Flow decreases with Vasoconstriction
      1. Decreases in vessel radius result in exponentially reduced flow (Poiseuille Equation)
      2. Arteriosclerosis with vessel narrowing also decreases flow
    3. Sympathetic-mediated Vasoconstriction selectively affects tissue perfusion
      1. Critical organs (heart, brain and skeletal Muscle) have increased Blood Flow (vasodilation)
      2. House-keeping organs (GI Tract, liver, Kidney, skin) have decreased Blood Flow (Vasoconstriction)
  5. Peripheral vascular response to local mediators
    1. Mediators of Arteriolar Dilation (and other vasodilation)
      1. Increased peripheral acid (Hydrogen Ion, carbon dioxide, Lactic Acid)
      2. Increased Electrolytes (magnesum, Potassium)
      3. Decreased Calcium
      4. Vasoactive agents (Adenosine, bradykinin, Histamine, nitric oxide)
      5. Increased Serum Osmolality
      6. Tissue Hypoxia
    2. Other mediators with mixed effects
      1. Prostaglandins
      2. Serotonins
  6. Baroreceptors
    1. Baroreceptor distribution
      1. Venous baroreceptors
      2. Cardiac baroreceptors
      3. Carotid Sinus Baroreceptor (via CN 9, Glossopharyngeal Nerve)
      4. Aortic Arch Sinus Baroreceptor (via CN 10, Vagus Nerve)
    2. Baroreceptors fire Nerve Impulses at baseline to suppress Blood Pressure
      1. Baroreceptors detect vascular pressure changes (Hypertension, Hypotension)
    3. Normal or high Blood Pressure (baroreceptors fire)
      1. Parasympathetic System is stimulated (e.g. Vagus Nerve stimulation)
      2. Sympathetic System inhibited (e.g. decreased Catecholamines, ADH)
    4. Hypotension (decreased baroreceptor firing)
      1. Parasympathetic System is suppressed (e.g. decreased Vagus Nerve activity)
      2. Sympathetic System is stimulated (e.g. increased Catecholamines, ADH)
    5. Baroreceptors (esp. carotid sinus) are sensitive to external pressure
      1. Carotid Sinus Massage is used as a Vagal Maneuver (e.g. PSVT) to slow Heart Rate
      2. Carotid Sinus Hypersensitivity may result in Cardioinhibitory Syncope
  1. Parasympathetic System
    1. Vagus Nerve
      1. Depresses Heart Rate (and to a lesser extent contractility) and Blood Pressure
  2. Sympathetic System
    1. Brain Stem and Hypothalamus stimulates Sympathetic Nerves to release Norepinephrine
      1. Vasoconstriction, esp. venous Vasoconstriction (Alpha 1 Adrenergic Receptor)
      2. Increased Heart Rate and contractility (Beta 1 Adrenergic Receptor)
      3. Unlike Epinephrine, Norepinephrine has no significant Beta 2 Adrenergic Receptors
    2. Adrenal Medulla is stimulated by Sympathetic Nerves to release norepinephine and Epinephrine
      1. EpinephrineVasoconstricts via Alpha 1 Adrenergic Receptors as does Norepinephrine
      2. Epinephrine (via Beta 2 Adrenergic Receptors) vasodilates vessels in heart and skeletal Muscle
    3. Kidney-based granular cells with Beta 1 Adrenergic Receptors are stimulated by Sympathetic System
      1. Factors stimulating Granular cell Renin release
        1. Sympathetic System stimulation (Beta 1 Adrenergic Receptors)
        2. Low Blood Pressure (direct effects)
        3. Macula Densa detects low Sodium concentration in the renal tubule
          1. Low Sodium in the renal tubule occurs in hypovolemic states with decreased GFR
          2. Renal tubule stasis allows for greater Sodium without water absorption
          3. Macula densa releases Prostaglandins in response
            1. Prostaglandins dilate renal afferent arteriole and increase GFR
            2. Prostaglandins stimulate renin release (increases Sodium AND water reabsorption)
      2. Renin secreted from renal granular cells and results in Angiotensin 2
        1. Renin converts Angiotensinogen to Angiotensin 1
        2. Angiotensin Converting Enzyme (ACE) in pulmonary capillaries converts Angiotensin 1 to 2
      3. Angiotensin 2 stimulates Vasoconstriction and Adrenal CortexAldosterone release
      4. Aldosterone stimulates Sodium (and water) reabsorption from renal tubules
  1. See Sodium and Water Homeostasis
  2. Images
    1. renalSodiumWaterHomeostasis.png
  3. Antidiuretic Hormone (ADH, Vasopressin)
    1. Mediators
      1. Released from Hypothalamus in response to increased Serum Osmolality
      2. ADH release is inhibited by Alcohol
    2. Effects
      1. Increases water reabsorption from renal tubules
      2. Increases Vasoconstriction and Peripheral Vascular Resistance
  4. Glomerulus
    1. Blood Pressure
      1. High pressures entering glomerulus (afferent arteriole) drive more fluid into urine
      2. Low Blood Pressures entering glomerulus result in retention of water
    2. Osmotic pressure
      1. Serum hypoosomolality (Fluid Overload) results in greater fluid gradient into urine
      2. Serum Hyperosmolality (Dehydration) attracts fluid back into circulation
      3. Serum contains large Proteins (esp. albumin) that do not normally cross the glomerulus
        1. Large Proteins maintain an osmotic pressure gradient into the serum
        2. In nephropathy (e.g. Nephrotic Syndrome), large Proteins do cross the glomerulus
          1. Resulting hypoproteinemia results in Interstitial Edema (following osmotic gradient)
    3. Glomerulus permeability
      1. Glomerular permeability decreases with decreased glomerular surface area
      2. Glomerular capillary Mesangial Cells contract in response to ADH and Angiotensin II
        1. On Mesangial Cell contraction, glomerular surface area is reduced
        2. Reduced glomerular surface area results in less fluid filtration across the glomerulus
  1. See Hypertension Management
  2. See Hypertensive Emergency
  3. Agents that modify fluid balance
    1. Diuretics (e.g. Loop Diuretics, Thiazide Diuretics)
      1. Block active transport of Sodium (and water) out of urine in loop of henle and renal tubule
      2. Results in increased excretion of Sodium and water, as well as Potassium
    2. Aldosterone Antagonist (e.g. Spironolactone, Eplerenone)
      1. Aldosterone blockade results in Sodium (and water) excretion, and Potassium retention
  4. Agents that modify vascular tone
    1. Sympathetic activity
      1. Alpha Adrenergic Central Agonist (e.g. Clonidine) inhibits sympathetic outflow
        1. Decreases Peripheral Vascular Resistance (via vasodilation) and decreases Heart Rate
      2. Alpha Adrenergic Antagonist (e.g. Terazosin, Prazosin)
        1. Block sympathetic stimulation of vascular Smooth Muscle resulting in vasodilation
    2. Direct Vasodilators
      1. Calcium Channel Blockers
        1. Inhibits Calcium influx into Smooth Muscle Cells resulting in vasodilation
    3. Renin-Angiotensin System
      1. Angiotensin Converting Enzyme Inhibitor (ACE Inhibitors)
        1. Blocking ACE activity (lungs), blocks conversion of Angiotensin 1 to Angiotensin 2
        2. Decreased Angiotensin 2 results in vasodilation and decreased Aldosterone release
      2. Angiotensin Receptor Blockers (ARB)
        1. Blocks Angiotensin 2 receptors with similar result as with ACE Inhibitors
  5. Agents that modify cardiac activity (contractility and Heart Rate)
    1. Beta-1 Adrenergic Antagonist or Beta Blockers (e.g. Metoprolol)
      1. Decrease cardiac contractility and Heart Rate
  1. See Shock
  2. Hemorrhagic Shock and Severe Dehydration
    1. Rapid volume replacement with the lost fluid type
  3. Septic Shock
    1. Fluid Resuscitation with large fluid volume bolus (typically 30 cc/kg)
    2. Vasopressors (e.g. Norepinephrine) when fluid Resuscitation fails to raise mean arterial pressure (MAP) > 65 mmHg
      1. Norepinephrine increases cardiac contractility and Vasoconstriction
    3. Identification of infection source and early use of antimicrobial agents
  4. Cardiogenic Shock
    1. Hypotension in Cardiogenic Shock is among the most difficult acute stabilization tasks
    2. Hypotension limits the typical CHF strategy of Preload reduction
      1. However, noninvasive Positive Pressure Ventilation (e.g. BIPAP) may be tolerated
      2. BiPAP reduces proload and improves oxygenation without a drop in circulating volume
    3. Vasopressors (sympathetic agents) are often required acutely
      1. Norepinephrine
        1. Beta 1 Adrenergic ReceptorAgonist (increased contractility)
        2. Alpha Adrenergic ReceptorAgonist (Vasoconstriction)
      2. Dobutamine
        1. Beta 1 Adrenergic Receptor (increased cardiac contractility and Heart Rate)
        2. Beta 2 Adrenergic Receptor (mild increase in vasodilation)
  • References
  1. Goldberg (2014) Clinical Physiology, Medmasters, p. 4-20
  2. Guyton and Hall (2006) Medical Physiology, p. 195-231