G3iii / G4vi / 25A03: Define systemic blood pressure and provide a formula that best describes its determinants

25A03: Exam Report

  1. Define systemic blood pressure and provide a formula that best describes its determinants (10% of marks).

  2. Describe the factors that determine systemic blood pressure (90% of marks).

76% of candidates passed this question.

  1. A definition of systemic blood pressure is found in most physiology textbooks and describes this as the pressure exerted on the arterial walls in the systemic circulation. It is a product of vascular resistance and blood flow. An expected formula would be: Pa-Pv (arterial venous pressure difference) = QR where Q is blood flow and R is peripheral arterial resistance. An alternative formula of MAP = CO X TPR was also accepted and provided a structure for the second part of the question.
  2. This section required a more detailed discussion of the factors in the equation including determinants of cardiac output, arterial blood volume, arterial elastance and peripheral arterial resistance (based on the Poiseuille equation). Your discussion should include naming the factor and then providing a description of how that factor increases/decreases or contributes to systemic blood pressure relating this to the formula provided in the first part of the question.

G3iii / G4vi / 25A03: Define systemic blood pressure and provide a formula that best describes its determinants

Answer

This was arguably one of the hardest questions in the 25A exam due to its depth and breadth. The key is to structure your question around an equation, stick to it, and explain each component as fast as you can.

You would be writing like crazy to get the following in 10 mins – but it is good practice for timing

THIS IS A QUESTION YOU NEED TO STICK TO TIME FOR – SO WRITE A HEADING ON EACH PAGE TO KEEP YOURSELF ON TRACK & WHEN IT GETS TO 10mins STOP!!!

By writing the headings you will give the examiner an idea of where you were heading and if your content is good for the headings you did complete, they will know you were going to write a solid answer (should give you a more favourable mark)

If you have time later come back and fill it in.

Remember: You need to answer every question – stick to time!!!

A

  • Systemic blood pressure = the pressure that blood exerts onto the arterial walls in the systemic circulation and excludes the pulmonary circulation.
  • MAP = (CO x SVR) + CVP
  • MAP is mean arterial pressure and is the primary pressure that drives blood flow into organs.
  • CO = cardiac output.
  • SVR = systemic vascular resistance.
  • CVP = central venous pressure and is assumed to be 0mmHg thus MAP = CO x SVR

B

SVR

  • The resistance to blood flow offered by all the systemic vasculature excluding pulmonary vasculature.
  • ↑SVR = ↑MAP
  • SVR = 10-20mmHg/L/min (10-20 Wood units) OR 800-1600 dynes.s/cm^5
  • Determined by changes to the vessel radius of arterioles as determines by Darcy’s law and the Hagen- Poiseuille law.

Darcys Law

\(\text{F} = \frac{\Delta P}{R}\)

HP EQN for R

\(R = \frac{8 \eta L}{\pi r^4}\)

Flow Rate

\(\text{Flow rate} = \frac{P \pi r^4}{8 \eta L}\)

  • Flow is indirectly proportional to resistance
  • P = pressure, r = radius ; Increase = Increase Flow = Decrease SVR
  • η = viscosity and L = length of the vessel; Increase = Decreased Flow = Increase SVR
  • This assumes laminar flow in a vessel.
    • Concentric layers of blood moving parallel to one another down a length of a blood vessel.
      • Orderly movement
      • Minimal energy losses
      • Fastest velocity in centre, slowest at endothelium
      • Most efficient form of flow (a)
    • Of all of these factors RADIUS is the most important determinant of SVR
    • Intrinsic and extrinsic factors affect the radius of arterioles
  1. Laminar flow
  2. Turbulant flow

Intrinsic Factors

Tissue Metabolites:

  • Produced by active metabolising tissues.
  • eg H+, phosphate, adenosine, ATP, ↑PaCO2, ↓PaO2, Lactate, K
  • All promote vasodilation = ↓SVR

Myogenic Autoregulation:

  • Increase in intravascular pressure in arterioles → stretch → VC → increase SVR
  • Reverse is true with
    ↓ intravascular pressure

Local paracrine hormones:

Vasodilatory:

  • Bradykinin, Histamine, PGE2
  • VD = ↓ SVR

Vasoconstriction:

  • Thromboxane, leukotrienes
  • VC = ↑SVR

Endothelial Factors:

  • NO, Prostacyclin = VD = ↓SVR

  • Endothelin-1 = VC = ­↑SVR

Extrinsic Factors:

Nervous System

Adrenergic SNS:

  • NA → VC (via Gq pathway) → increase SVR → increase MAP

Cholinergic SNS:

  • Generally, causes vasodilation in skeletal muscle beds only → decrease SVR.

Humoral Factors

Adrenaline

  • Beta2-AR → VD → decrease SVR (via Gs) → increase MAP

Noradrenaline

  • Alpha1-AR → VC → increase in SVR (via Gq) → increase MAP

Vasopressin

  • From posterior pituitary
    Via V1 receptors (Gq mediated) → VC → increase SVR → increased MAP

AT-II
Via RAAS
VC via AT1-R (Gq) → increase SVR → increase MAP

Natriuretic peptides

  • ANP:
    Released by atrial distension
    Decreases renin release → decreased RAAS → decreased ATII → decreased VC → decrease SVR → decreased MAP (indirectly).

CO

  • CO = SV x HR and is the amount of blood pumped by the left ventricle per minute.
  • CO = 5-6L/min

SV = EDV - ESV

  • Volume of blood ejected into the aorta each beat and is dependent on preload, afterload and contractility.
  • An increase in SV → increase in CO → increase in MAP and vice versa.

Factors that influence SV = PreL, AfterL, C

Contractility (Inotropy):

  • The intrinsic ability of the myocardial cells to develop force given a fibre length independent of preload and afterload.
  • Increased contractility → increased SV → increased CO → increased MAP and vice versa
  • Factors increasing inotropy:
    • Sympathetic activity & Circulating catecholamines
      • NA from SNS on β1 AR on cardiac myocytes
    • Anrep Effect
      • Abrupt increase in afterload increases inotropy
      • Intrinsic to heart
    • Bowditch Effect (aka Treppe phenomenon)
      • Increase in HR → increase in inotropy
Factors increasing ventricular inotropy diagram.

Preload:

  • The stretch of cardiac myocytes prior to contraction; it is related to the sarcomere length at the end of diastole
  • LVEDP/LVEDV used as indirect indices as sarcomere length cannot be measured.
  • Increased preload → increased SV → increased CO → increased MAP
  • Factors increasing preload:
    • Increased CVP
      • Increased venous blood volume
        • Increased total blood volume
        • Increased venous return
          • venoconstriction → decreased venous compliance → increased VR
        • Increased Ventricular compliance
          • Greater the compliance, greater the ventricular filling
        • Increased Atrial inotropy
          • Increases ventricular filling
          • At higher HR, less diastolic filling time.
            • Increased atrial inotropy remedies this.
          • Increased outflow resistance and afterload
          • Decreased HR
            • Increased ventricular filling time (to an extent)
            • Lost in AF with rVr
          • Decreased ventricular inotropy = higher LVEDV
Diagram of factors affecting ventricular preload in heart.

Afterload:

  • The load against which the heart must contract to eject blood.
  • Increased afterload → decreased SV → decreased CO → decreased MAP
  • Afterload estimated by ventricular wall stress (σ).
  • \(\sigma \propto \frac{P \cdot r}{h}\)
  • P = intraventricular pressure
    • Increased pressure → increased wall stress (afterload) → decreased SV
  • R = ventricular radius
    • Increased radius → increased afterload → decreased SV
  • H = wall thickness
    • Decreased wall thickness → increased afterload → decreased SV
  •  

HR:

  • Changes in HR more important quantitatively in producing changes to CO than SV
  • Brought about by changes in sympathetic and parasympathetic nerve activity at the SA node.
  • Extreme Tachycardia (VT, AF with rVr).
    • Decrease in length of diastole → decreased ventricular filling time → fall in SV → decreased CO
  • Extreme bradycardia also decreased CO due to simply fewer bpm thus → decreased CO
  • Many factors affecting HR:
    • Hormones
    • Drugs
    • Temperature
    • Electrolyte levels
    • Ischaemia/hypoxia

Arterial Compliance / Elastance

  • Elastance: stiffness of arterial tree; ↑ stiffness → ↑ systolic BP, ↓ diastolic runoff
  • Influenced by age (arterial stiffening), atherosclerosis, hypertension, connective tissue disease

Arterial Blood Volume

  • Intravascular volume status: determines mean systemic filling pressure → venous return → preload → CO
  • Modulated by renal function, RAAS, ADH, natriuretic peptides, external losses (haemorrhage, dehydration)

Anrep Effect

  • Mechanism of cardiac compensation due to an increase in end systolic volume & reduced SV brought on by an increase in SVR
  • Sustained myocardial stretch (higher end systolic volume)
  • Activation of tension-dependant Na/H exchangers
  • Increased [Na] in sarcolemma
  • Stops activity of Na+-Ca++ exchanger
  • Increase [Ca++] in sarcolemma

Sources:

  • Cardiovascular Physiology Concepts (Klabunde, 3rd edition) – Not a formal prescribed text but an amazing resource. I didn’t use Pappano.
  • Kam and Power (4th Edition)

 

Author: Alex Fagarasan