Cardiovascular Control System (Ramchandra) Flashcards

1
Q

Effector mechanisms responsible for regulating cardiovascular function include…..

A
  • Sympathetic and parasympathetic outflow from autonomic nervous system to heart and blood vessels;
  • Components of neuro-endocrine system including
    • Catecholamines released from the adrenal medulla
    • Renin angiotensin system
    • Antidiuretic hormone (ADH)
    • Natriuretic peptides
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2
Q

What increases the release of renin from the kidneys?

A

1) Increase sympathetic nervous system
2) When a fall in arterial blood pressure is detected by pressure sensitive receptors (baroreceptors) in the arterial vessels.
3) When a decrease in sodium chloride (salt) is detected in the kidney by the macula densa in the juxtaglomerular apparatus.

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3
Q

Describe the RAA System

A
  • Liver produces Angiotensinogen
  • The juxtaglomerular apparatus produces renin
    • Stimulated by decrease in renal perfusion
  • Renin converts angiotensinogen to angiotensin I
  • ACE is released from the surface of the pulmonary and renal endothelium
  • ACE converts Angiotensin I to Angiotensin II
    • ​Causes water and salt retension. Effective circulating volume increases. Perfusion of the juxtaglomerular apparatus increases.
  • Angiotensin II does the following
    • Increase sympathetic activity
    • Increase tubular Na+ and Cl- reabosption and K+ excretion. Therefore results in H2O retension
    • Increases Aldosterone secretion from the adrenal gland cortex. ALso results in H2O retension
    • Increases arteriolar vasoconstriction which causes increase in BP
    • Increases ADH secretion from the pitutiary gland (posterior lobe)
      • ADH causes H2O absoption from the collecting dcut
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4
Q

Describe the location of arterial barorecetprors

A

Anatomy of Systemic Arterial Baroreceptors

  • The main groups of systemic arterial baroreceptors are found in the carotid sinus (cranial nerve IX or glossopharyngeal nerve) and aortic arch (cranial nerve X).
  • Other receptors are distributed along the common carotid and subclavian arteries. Their afferents also join cranial nerve X.
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5
Q

What are the baroreceptors responding to?

A

Stretch of the arterial wall and the intraluminal pressure (difference between inside vs outside pressure)

Systemic arterial baroreceptors give rise to both myelinated (fast-conducting) and unmyelinated (slow- conducting) afferents and also receive efferent innervation. The response of the carotid sinus baroreceptors has been well characterized.

The relationship between carotid sinus pressure and afferent nerve activity exhibits the following:

  • Threshold: below 30-50 mmHg, a decrease in pressure does not alter the firing rate
  • Saturation: an increase in pressure above 150-180 mmHg also has no further effect on firing frequency
  • Rate sensitivity: for a given mean pressure the rate of firing is greater for pulsatile pressure than for steady pressure.
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6
Q

Describe the Systemmimc Arterial Baroreceptors reflex

A

Systemic Arterial Baroreceptors Reflex

Systemic arterial baroreceptors are classified as slowly adapting receptors.

  • That is, if a s_teady pressure is applied t_o the arteries there will be a sustained increase in firing rate for at least an hour.
  • Over a period of hours to days, however, adaptation will occur and firing rates will fall back to control levels.

Information is also sent to the brain about the pulsatile nature of the heart beat = info up to the brain is saying what the difference is between systolic and diastolic pressure. As well as the t_onic level of the blood pressure_ (as the BP increases, pulses increaes)

As the blood pressure goes up, vagal activity also goes up. As the BP goes up, smypathetic cardiac nerve activity goes down.

The firing response of systemic arterial pressure receptors is modulated by external neural factors and local paracrine effects.

Changes in arterial baroreceptor firing rates give rise to characteristic “reflex” responses. Extent of these reflex adjustments is graded with respect to the change in pressure.

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7
Q

Describe the characterisitics of the carotid sinus baroreceptors that affect its responses

A
  • Threshold: below 30-50 mmHg, a decrease in pressure does not alter the firing rate
  • Saturation: an increase in pressure above 150-180 mmHg also has no further effect on firing frequency
  • _Rate sensitivity**_: for a given mean pressure the r_ate of firing_ is greater for pulsatile pressure than for steady pressure.
    • =How well are the increases in BP buffered by the barorecptor reflex?
    • _​If the slope is le_ss steep, you’re more likely to have increased pressure with less baroreceptor reflex
    • This is important clinically, because we used to be interested in the mean/stable BP. In addition to the basic tonic BP, it is the increases and decreases in pressure that determines somone’s risk of stroke. (e.g. it is more dangerous for someone with mild hypertension that have occasionally v. high hypertension than someone with constantly high hypertension)
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8
Q

When the arterial pressure falls, the following occur

A
  1. Increased HR and cardiac inotropic state
  2. Graded constriction of precapillary resistance vessels in skeletal muscle, splanchnic, cutaneous and renal criculations- this does not occur in crerebral or coronary circulations
  3. Venoconstriction
  4. Increased catecholamine secretion by adrenal medulla ALSO Increased circulating levels of ADH, AII and other hormones
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9
Q

Where are the cardiac receptors with Myelinated Vagal Afferents found?

What are these receptors senstiive to?

A

Cardiac receptors with myelinated vagal afferents (rapidly conducting fibres) are located in subendocardial tissue, principally at veno-atrial junctions.

  • These receptors are sensitive to the filling of the highly compliant atrial chambers.
  • They emit bursts of firing synchronous with _‘a’ wave (_atrial contraction) of atrial pressure; or fire late in ventricular systole (corresponding to the ‘v’ wave in the atrial pressure trace), where atrial filling is most complete.

Cardiac receptors therefore provide afferent information on the extent of cardiac filling and are directly influenced by changes in venous return and blood volume.

For this reason, they are viewed as low-pressure or volume receptors.

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10
Q

Describe the Cardiac Receptors Responses

A

Responses to altered cardiac receptor firing are qualitatively similar to those described above for systemic arterial baroreceptors.

That is, i_ncrease in cardiac filling_ leads to i_ncreased firing (step activation) of myelinated RA receptors, which leads to…._

  • Increased HR (?)- vein bridge reflex
  • Reduced renal sympathetic stimulation

Increased aggregate activation of cardiac receptors qalitatively similar systemic arterial baroreceptor reflex responses.

However, there are some quantitative differences.

  • It has been argued that activation of cardiac receptors has a more powerful effect on neurohumoral systems associated with extracellular fluid volume regulation (ADH and angiotensin II)
  • Also, rapid volume loading of heart may cause a transient elevation of heart rate, which is called Bainbridge reflex (try to unload volume).
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11
Q

Describet he Osmoreceptors

A

Osmoreceptors in the supraoptic and paraventricular nuclei of hypothalamus sense changes in effective plasma osmolality by altering their volume.

This modulates sensory output from these cells that control synthesis and release of ADH by posterior pituitary gland.

  • Reduced ADH secretion d_ecreases water reabsorption_ and leads to the excretion of dilute urine by the kidney. The opposite occurs when ADH concentration rises.
  • In addition to these affects, ADH is also a potent vasoconstrictor, hence its other name vasopressin.
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12
Q

Describe Chemoreceptors

A

Peripheral chemoreceptors in aortic and carotid bodies, and central chemoreceptors in the hindbrain play a major role in regulating blood chemistry. They are closely linked with control of respiratory function.

  • Generally, chemoreceptors respond to increased PaCO2, H+ concentration, and decreased PaO2.
  • Increased discharge of peripheral chemoreceptors brought about by low PaO2, stimulates increased sympathetic drive to heart and vessels. When oxygen delivery is compromised e.g. by reduced arterial pressure, chemoreceptor activation causes vasoconstriction and constributes to restoration of blood pressure
  • However, for peripheral chemoreceptors, latter response is most important physiologically. Decreased PaO2 leads to increased discharge of peripheral chemoreceptors, which then stimulates increased sympathetic drive to heart and vessels.

When oxygen delivery to rapidly metabolising chemoreceptors is compromised (e.g. due to decreased arterial pressure below 60-70 mmHg), chemoreceptors are stimulated. This causes heart rate reduction and a generalised vasoconstriction of resistance vessels, which contributes to restoration of blood pressure.

In some heart failure/hypertensive patients, increased chemoreceptor drive may be responsible for increases in sympathetic activity.

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13
Q

Describe the Cardiovascular Control in the brainstem (when there’s increased arterial pressure)

A

It has long been known that neural circuitry necessary to preserve reflex control of arterial pressure is located at a more primitive level of the brain, i.e. in the medulla oblongata and brainstem.

Discrete groups of neurons in ventrolateral region of the medulla oblongata responsible for tonic activity and r_eflex control_ of autonomic nerves (supplying heart and blood vessels) are identified in figure 5.

The proposed neural wiring provides a basis for observed reflex responses to sudden changes in systemic arterial pressure.

  • Increased arterial pressure leads directly to increased afferent activity in CN 9/10 and increased activity in NTS as a result.
  • This stimulates both CVN (cervical vagus nerve) and the CVLM (caudal ventrolateral medulla).
    • Increased CVN activity boosts parasympathetic drive to heart.
    • Increased CVLM activity inhibits tonic activity of RVLM (Rostral ventrolateral medulla), reducing sympathetic outflow to heart and circulation.
  • This results in decreased heart rate and decreased cardiac inotropic state, combined with vasodilation.
  • Ultimately, this will tend to correct the initial increase in systemic arterial pressure.

“If you have increased baroreceptor afferent activity, the inhibitory pathway causes reduction in sympathetic nervous activity. For vagal activity, there is no inhibitory pathway so if the pressure goes up, so does the vagal activity.”

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14
Q

Which baroreceptors are innervated by which nerves?

A

The main groups of systemic arterial baroreceptors are found in the carotid sinus (cranial nerve IX or glossopharyngeal nerve) and aortic arch (cranial nerve X).

Other receptors are distributed along the common carotid and subclavian arteries. Their afferents also join cranial nerve X.

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15
Q

What happens as arterial pressure increases?

A
  • Carotid nerve impuses
    • Increases frequency
  • Vagus nerve impuses
    • Increases frequency
  • Sympathetic carotid nerve
    • Decreases impuses
  • Heart rate
    • Slows down
  • Contractility
    • Decreased
  • Sympathetic vasoconstrictor nerves
    • Decreased frequency
    • Decreased vasoconstriction.
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16
Q

What nerves innervates the cadiac receptors?

A

Cardiac receptors with myelinated vagal afferents (rapidly conducting fibres) are located in subendocardial tissue, principally at veno-atrial junctions.

Unmyelinated C-Fibre Afferents

In addition, there are unmyelinated C-fibre afferents throughout all four cardiac chambers. The density of these cardiac vagal afferents is much greater than myelinated cardiac vagal afferents.

  • In resting conditions, unmyelinated receptors have a sparse and irregular discharge
  • With increased cardiac filling, their aggregate output increases markedly.
17
Q

Describe the Cardiac receptor responses

A

Cardiac Receptors Responses

Responses to altered cardiac receptor firing are qualitatively similar to those described above for systemic arterial baroreceptors.

That is, increase in cardiac filling leads to increased firing (step activation) of myelinated RA receptors:

  • Reduced sympathetic outflow to heart and vessels,
  • Increased cardiac vagal activity,
  • Reduced catecholamine secretion by the adrenal medulla
  • Decrease in circulating levels of ADH and angiotensin II (decreased renal sympathetic stimulation).

However, there are some quantitative differences.

  • It has been argued that activation of cardiac receptors has a more powerful effect on neurohumoral systems associated with extracellular fluid volume regulation (ADH and angiotensin II)
  • Also, rapid volume loading of heart may cause a transient elevation of heart rate, which is called Bainbridge reflex (try to unload volume).
18
Q

Describe the CNS ischaemic response

A

When arterial pressure falls to levels at which cerebral perfusion is compromised, hypoxia and hypercapnia activate vasomotor neurons in ventrolateral medulla and hypoxia excites the cardiac vagal nuclei (CVN).

  • This results in increased sympathetic outflow, which causes intense vasoconstriction and the release of large quantities of catecholamines from the adrenal medulla.
  • In addition, increased cardiac vagal activity r_educes heart rate._