Why is it important to minimise fluctuations in blood pressure?

The organs require a fairly constant mean arterial pressure (MAP) to ensure adequate perfusion. Some organs (most notably the brain, heart and kidneys), despite fluctuations in MAP, intrinsically maintain their blood flow through autoregulation (see Chapter 34), but are still unable to compensate if MAP is significantly reduced or increased.

How is MAP kept constant?

Normal activities (including changes in body position, exercise and digestion) can potentially result in major changes in MAP, as they can cause both vasodilatation or vasoconstriction of vascular beds and can increase or decrease venous return to the heart. The cardiovascular system rapidly responds to fluctuations in MAP through a series of neural reflexes. These cardiovascular reflexes may be classified as:

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  Reflexes originating from stimuli within the cardiovascular system:

  
  
  
  
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     – The arterial baroreceptor reflex. Changes in MAP are detected by mechanoreceptors in the aortic arch and carotid sinus. In response, sympathetic outflow from the central nervous system (CNS) is rapidly altered, which in turn modifies heart rate (HR) and systemic vascular resistance (SVR), returning MAP to its set point. This is the major cardiovascular reflex involved in short-term control of MAP.

     
     
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     – The Bainbridge reflex, in which an increase in central venous pressure (CVP) results in an isolated tachycardia.

     
     
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     – The chemoreceptor reflex, in which activation of the peripheral chemoreceptors triggers an increase in sympathetic nervous activity, thus increasing HR and MAP under conditions of extreme hypotension and cardiovascular collapse. This reflex is only usually relevant during profound hypotension, such as during haemorrhage or sepsis.

     
     
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     – The CNS ischaemic response, in which CNS ischaemia triggers an increase in sympathetic nervous activity, thus increasing HR and MAP.

  
  
  
  
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  Reflexes triggered by stimuli external to the cardiovascular system: for example, pain, emotion or temperature.

Describe the arterial baroreceptor reflex

The arterial baroreceptor reflex is an extremely important mechanism for minimising fluctuations in MAP. The arterial baroreceptors are mechanoreceptors that sense the degree of distension of the walls of the carotid sinus, a dilatation at the bifurcation of the carotid artery and the aortic arch (of lesser importance):

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  An increase in MAP distends the wall of the carotid sinus/aortic arch, which increases the frequency of action potentials generated by the baroreceptor afferent fibres.

  
  
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  A decrease in MAP reduces carotid sinus/aortic arch wall distension, which decreases the frequency of action potential generation.

The baroreceptors transmit their action potentials to the vasomotor centre, located in the medulla oblongata, through the glossopharyngeal nerve (carotid sinus baroreceptors) and the vagus nerve (aortic arch baroreceptors). The vasomotor centre is divided into two functional areas:

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  The vasoconstrictor (pressor/defence) area. This area triggers tachycardia, increased myocardial contractility and vaso- and veno-constriction and promotes adrenaline release from the adrenal medulla through sympathetic efferent neurons.

  
  
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  The vasodilator (depressor) area. This area acts on the vasoconstrictor centre, decreasing its sympathetic outflow.

Overall:

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  An increase in MAP increases the frequency of action potentials produced by the baroreceptors. In response, the vasodilator area inhibits sympathetic outflow, causing peripheral vasodilatation and a decrease in both HR and myocardial contractility, thus returning MAP to normal.

  
  
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  A decrease in MAP reduces the frequency of action potentials produced by the baroreceptors. In response, the vasoconstrictor area increases sympathetic outflow, causing peripheral vasoconstriction and an increase in both HR and myocardial contractility, thus returning MAP to normal.

Some important points to note about this system are:

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  In addition to short-term changes in HR, myocardial contractility and SVR, the baroreceptor reflex also influences plasma volume. Following a fall in MAP, the increased sympathetic outflow triggers renin secretion by the kidney, thus increasing plasma volume through the action of the renin–angiotensin–aldosterone (RAA) axis. Likewise, an increase in MAP decreases sympathetic outflow, which decreases renin secretion and thus plasma volume. In clinical practice, this can be observed in patients with pre-eclampsia, where persistently raised MAP results in a relative hypovolaemia.

  
  
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  There are two types of neurons involved in the baroreceptor reflex. Large myelinated A fibres are activated at lower pressure, whilst small unmyelinated C fibres are activated at higher pressure. In combination, these neurons provide a system that is sensitive over a wide range of MAP, from 80 to 150 mmHg.

  
  
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  In patients with chronic hypertension, the baroreceptors reset their working range and sensitivity.

  
  
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  The compliance of the arterial tree is reduced with ageing and atherosclerosis. In turn, this affects the sensitivity and rapidity of the baroreceptor reflex; postural hypotension (i.e. a failure of the baroreceptor reflex to compensate for the postural changes in MAP) is common in the elderly.

What is the Bainbridge reflex?

Low-pressure mechanoreceptors are located within the great veins and the walls of the right atrium (RA) at its junction with the superior and inferior venae cavae and are activated by increased wall distension. An increase in CVP therefore stimulates these low-pressure mechanoreceptors, increasing their frequency of action potential generation – these action potentials are then relayed to the CNS via the vagus nerve. In response, the vasomotor centre increases sympathetic outflow to the sinoatrial node (but not to the cardiac ventricles or peripheral vasculature), resulting in an isolated tachycardia.

Physiological manifestations of the Bainbridge reflex are:

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  Respiratory sinus arrhythmia. This occurs in children and young adults. During inspiration, negative intrathoracic pressure leads to a transient increase in venous return to the RA, which activates low-pressure mechanoreceptors. As a result, HR increases during inspiration and decreases during expiration.

  
  
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  Uterine autotransfusion. Following delivery, sustained uterine contraction returns around 500 mL of uteroplacental blood to the maternal circulation. The resulting increase in CVP stretches the right atrial wall, resulting in a tachycardia.