The two circulations in the body are the pulmonary and systemic circulations.
The right side of the heart delivers blood to the pulmonary circulation, to partake in gas exchange. The left side of the heart delivers oxygenated blood onto the rest of the body.
The human body has approximately 65-75ml/kg of blood, depending on whether adult/child, male/female. This gives approximately 5 or so litres of blood for an average adult.
Pulmonary circulation
The pulmonary circulation receives the entire cardiac output via the right ventricle, holding approximately 10% of the total blood at any time. It is a low pressure (approx 25/8 mmHg / mean PAP 15 mmHg), high surface area, highly elastic, thin walled network of blood vessels.
Blood flow can be altered by:
- Gravity (higher blood flow and perfusion at the lung bases due to gravity),
- Pulmonary vascular resistance:
- Hypoxia, hypercapnia and acidosis (causes local vasoconstriction to divert blood to ventilated areas of lung, improving V/Q mismatch)
- Alveolar pressure and lung volume (alveolar recruitment expands blood vessels by tethering and traction, but can compress them if this expansion becomes excessive eg high PEEP in an intubated patient)
- Alpha-mediated sympathetic vasoconstriction of pulmonary blood vessels
- Pulmonary hypertension; such as cor pulmonale, acute hypertension from pulmonary embolism, left ventricular failure causing congestion etc
The ultra-thin vessel walls allow easy gas exchange, but can also result in fluid shifts and pulmonary oedema if hydrostatic pressures become excessive (such as in left ventricular failure).
Systemic circulation
The remaining 90% of blood is situated in the systemic circulation, with the majority of this volume located in the venous system (approximately 70%). The systemic circulation is characterised as a high pressure (approx 120/80 mmHg / MAP 90 mmHg), high resistance, thick-walled and less compliant network. Unlike the pulmonary system, systemic vessels respond to hypoxia and hypercapnia by vasodilation, in order to increase blood flow to replenish O2 and clear CO2.
The arterioles constrict and dilate to regulate blood flow to the capillaries supplying downstream tissue demands. The sum of these regional resistances contribute to the total systemic vascular resistance. The venous system, specifically veins and venules, act as a capacitance reservoir; the vast majority of blood in the body is located here (around 70%). This volume contributes to blood pressure by regulating venous return via volume and venoconstriction/dilation.
Why is arterial pressure so high?
We know that the right heart pumps blood around the lungs with a pressure around 20/10 mmHg, so why does the systemic pressure need to be circa 120/80?
Maintaining a higher systemic arterial blood pressure allows easier regulation of blood flow to the regions that need it, simply by fine-tuning arteriolar radius in the specific area to match demand. Vasodilation of a specified area with higher demand is much easier than vasoconstricting all other areas of vasculature in order to perfuse that area of raised demand.
A higher systemic blood pressure is also required to overcome gravitational forces; being bipedal and upright creates a hydrostatic gradient, necessitating a high enough blood pressure to enable blood flow to reach the lofty heights of the brain. A giraffe, by comparison, has a MAP of around 250 mmHg (versus an average human MAP of 90 mmHg).
This is also why an arterial line transducer should be placed at the level of the heart; in order to best reflect the pressures centrally. Placing it too low or high may inadvertently raise or lower the blood pressure readings, respectively, due to differences in hydrostatic pressure.
Systemic Vascular Resistance (SVR) & Regional Vascular Resistance (RVR)
We now circle back to the MAP equation in order to focus on the second component of MAP:
MAP = CO x SVR
SVR is the resistance within the systemic circulation, and is a major determinant of the afterload against which the left ventricle must pump.
Pouisueille’s law states that the flow of a liquid depends on its viscosity, and the length and diameter of the tube through which it flows. Although blood viscosity can be affected by haematocrit, fluid administration, lipid/protein plasma concentration and so on, since blood viscosity and vessel length don’t significantly alter in the short term, the primary modifiable factor for resistance is vessel radius, specifically in the arterioles. Small alterations in arteriolar radius result in large changes in resistance and, thus, flow.
Resistance is inversely proportional to the fourth power of the radius.
The regulation of tissue perfusion takes place at the level of the arterioles, mediated by vessel radius in response to local regulatory mechanisms. The arterioles lead directly to capillary vascular beds, the ‘business end’ where perfusion takes place. Each organ and tissue throughout the body will vary in their metabolic demands, and the resistance within each of these regions will dynamically fluctuate in order to match these demands.
Arterioles vasodilate in response to reduced perfusion pressure in order to minimise hypoperfusion and ischaemia. Conversely, higher perfusion pressures cause vasoconstriction to limit the risk of hyperperfusion. These dynamic compensatory changes may be affected by atherosclerosis, vessel stiffness, chronic hypertension, hyperglycaemia and glycation end products, medications, inflammatory factors, and so on. So there is considerable heterogeneity across different patient groups’ ability to maintain adequate tissue perfusion with the same blood pressure number on the screen.
Systemic vascular resistance (SVR) represents the overall resistance in the systemic circulation, and is essentially the net sum of these regional vascular resistances (RVR).
Changes in RVR across regions can significantly alter overall SVR, whereas smaller local RVR changes have negligible effects on overall SVR. RVR across the muscles, splanchnic vasculature and skin is the primary determinant of overall SVR, due to the large total area of these regions.
Whilst regional control of perfusion is variable, it still relies on an adequate overall MAP to allow autoregulation. Once MAP falls below the lower limit of autoregulation, regional blood flow becomes linearly dependent on MAP. The hypoperfusive troponin rise of a type 2 MI results from an inadequate MAP; in the case of traumatic brain injury bleed, MAP must be kept high enough to perfuse brain tissue against the opposing gradient of intracerebral pressure.
How do the arterial and venous systems differ in their effects on pressure?
SVR is primarily dictated by the arterial system, with the additive sum of arterioles in different RVR regions contributing to overall SVR. The venous system, however, is a high capacitance system (large volume, low resistance), that can recruit blood from unstressed into stressed volume, increasing MSFP, raising venous return, and ultimately increasing cardiac output and MAP.
Arteriolar constriction raises SVR, whereas venous constriction increases preload and cardiac output.
Determinants of systemic vascular resistance:
- Baroreceptor reflex; increased vagal tone to increased aortic/carotid sinus stretch will reduce sympathetic tone and SVR.
- Chemoreceptor reflex; systemic circulation hypoxia and/or hypercapnia can increase sympathetic tone and, thus, SVR.
- Circulating hormones; catecholamines such as cortisol and adrenaline, as well as angiotensin II and vasopressin, increase sympathetic tone and SVR
- RAAS – triggered by renal hypoperfusion, low Na to macular densa, and sympathetic activation (B1 receptors). ↑ RAAS activation causes ↑ SVR and ↑ sodium and water retention, leading overall to ↑ BP.
- ADH/vasopressin – released by posterior pituitary due to hypovolaemia or hyperosmolality. Causes vasoconstriction (V1 receptors) + water retention (V2 receptors in kidneys).
- ANP and BNP -triggered by atrial (ANP) and ventricular (BNP) stretch, leads to vasodilation / diuresis / natriuresis.
- Temperature; higher body temperatures cause vasodilation as a cooling measure, which can reduce SVR. Hypothermia causes vasoconstriction to conserve heat, which can raise SVR.
- Neural; there is a rich sympathetic supply to the arterial and venous system throughout the body, with activation of a1 receptors by noradrenaline or adrenaline causing vasoconstriction.
Determinants of regional vascular resistance (will affect the sum SVR):
- Regional mechanisms may over-ride baroreceptor effects at the local level; eg ↓ SVR during exercise may ↑ baroreceptor response → ↑ systemic vasoconstriction; however the exercising muscles may remain dilated due to demand and local mechanisms.
- Myogenic – increased stretch of the vessel wall directly triggers a reflex vascoconstriction, in order to protect downstream capillaries and tissues from hyperperfusion. This raises local, not systemic vascular resistance, since it is a regional response.
- Metabolic – metabolic end-products cause vasodilation locally in order to promote removal of these products, and replenishing of oxygen and energy substrates. CO2, lactate, histamine, potassium, hydogen ions, adenosine are some substances that locally vasodilate arterioles.
- Shear stress – increased dilation of distal arterioles due to demands of that specific region result in greater flow and shear stress in the vessel walls proximal to this. Endothelial mediators such as nitric oxide are released to vasodilate this area.
Local regulatory mechanisms can become dysregulated and lost in pathological states such as sepsis, resulting in decoupled macro and microcirculatory balance and subsequent compromised tissue perfusion.
Next up is looking more closely at the reflexes and neurological control of haemodynamics.