L01 CVS Control of blood pressure_shock

Overview

This lecture introduces mean arterial blood pressure (MABP) as the tightly regulated variable that drives tissue perfusion, then uses a trauma case (John Doe) to show how the baroreceptor reflex and fluid-shift mechanisms defend MABP after blood loss, how shock is classified by which determinant of MABP has failed, and why compensation eventually fails as losses become severe.

Blood pressure and why it matters

• BP drives tissue perfusion: it supplies O2 and nutrients and removes CO2 and H+.
• BP fluctuates continuously with each cardiac cycle (pulsatile pressure curve: a systolic peak, an incisura/dicrotic notch on the downstroke, and a diastolic trough), but mean arterial blood pressure (MABP) is the variable that is monitored and kept constant.
• $MABP=CO\times TPR$, and $CO=HR\times SV$.
• Low BP (shock) is a serious problem because it means inadequate tissue perfusion.
• MABP is monitored via baroreceptors; HR, SV and TPR are the variables altered to keep MABP constant. Significant problems with any of HR, SV or TPR can overwhelm this control and cause shock.

Baroreceptor reflex

• Baroreceptors are mechanoreceptors stimulated by stretch, located at the carotid sinus and the aortic arch.
• Afferents from the carotid sinus run via the carotid sinus nerve into the glossopharyngeal (IX) nerve; afferents from the aortic arch baroreceptors run via the vagus (X) nerve. Both send a constant signal to CVS centres in the brainstem.
• General reflex arc: a change in MABP alters baroreceptor firing, producing reflex outputs via the autonomic nervous system that adjust SV, HR and TPR to restore MABP. This operates constantly, e.g. to compensate for postural change (lying to standing).
• Detailed efferent pathway, as triggered by a fall in arterial pressure (e.g. haemorrhage): decreased firing by arterial baroreceptors produces four parallel outputs:
  1. Decreased parasympathetic discharge to the SA node -> increased heart rate (HR).
  2. Increased sympathetic discharge to cardiac muscle -> increased stroke volume (SV), toward normal.
  3. Increased sympathetic discharge to peripheral veins -> venoconstriction -> increased venous pressure -> increased venous return -> increased end-diastolic volume -> further increases SV.
  4. Increased sympathetic discharge to arterioles -> arteriolar constriction -> increased total peripheral resistance (TPR).
     HR and SV combine to increase cardiac output (CO); CO and TPR combine to increase arterial pressure back toward normal (MABP restored).
• If problems with the determinants of MABP (CO via HR/SV, and TPR) are severe enough, the reflex may not be able to compensate for the fall in MABP, leading to persistent hypotension, i.e. shock.

Shock: definition and classification

• Definition: reduced (inadequate) perfusion of tissues with blood, causing decreased delivery of O2 and other nutrients, leading to generalised tissue hypoxia, which if prolonged may cause irreversible cellular damage.
• Three classes, defined by which determinant of MABP has failed:
  • Hypovolaemic: decreased filling due to decreased volume (decreased preload).
  • Distributive: widespread vasodilation (decreased afterload).
  • Cardiogenic: decreased output, from a functional problem or an obstruction (decreased cardiac output).
• Causes within each class:
  • Hypovolaemic: loss of blood, plasma, or water and electrolytes. External losses - haemorrhage, burns, diarrhoea, vomiting, diuresis. Internal losses - crush injury, extravasation.
  • Distributive: generalised vasodilation where vascular capacity exceeds blood volume.
    • Anaphylaxis: immune reaction releasing histamine, marked peripheral vasodilation, +/- increased capillary permeability, decreased circulating volume.
    • Septic: marked inflammatory response with chemically mediated vasodilation, increased vascular permeability, platelet aggregation.
    • Neurogenic: loss of sympathetic vasomotor tone, from cervical spinal cord injury, decreased central vasomotor control, or anaesthesia.
  • Cardiogenic: decreased cardiac output from pump failure (infarction, arrhythmia, valve disease, myocardial depression) or extracardiac obstruction (cardiac tamponade, pneumothorax, pulmonary embolism).

Haemorrhage and hypotension: compensatory responses

• Haemorrhage rapidly lowers MABP (this is what happened to John Doe, producing marked hypotension).
• The fall in MABP triggers three homeostatic reflexes, on different timescales, to minimise the fall:
  1. Immediate - the baroreceptor reflex (as above).
  2. Intermediate - fluid shift from tissues into capillaries (“autotransfusion”).
  3. Long term - replacement of fluid and red cells.
• Intermediate mechanism (autotransfusion): the fall in arterial pressure drives the baroreceptor reflex, causing arteriolar constriction; this reduces capillary hydrostatic pressure, which increases fluid absorption from the interstitial compartment into the capillaries, increasing plasma volume and helping restore arterial pressure toward normal.
• Long-term mechanism (volume replacement):
  • ADH release, causing water retention.
  • Reduced renal perfusion activates the renin-angiotensin-aldosterone system (RAA), causing retention of Na+ and water.
  • Thirst.

Hypovolaemic shock: compensated stage (<10% blood loss)

• Blood pressure compensation: reduced MABP decreases baroreceptor activity, activating pressor areas in the CNS, which causes:
  • Arteriolar vasoconstriction, raising TPR and lowering renal blood flow/urine output.
  • Increased HR and myocardial contractility, raising CO and MABP toward normal.
  • Venoconstriction, raising venous return, SV and CO, and MABP toward normal.
• Volume compensation:
  • Arteriolar constriction lowers capillary pressure, causing fluid reabsorption (trans-capillary fluid shift).
  • Lower atrial pressure triggers ADH release, reducing water loss.
  • Lower renal perfusion activates the renin-angiotensin-aldosterone system, reducing renal sodium/water excretion.
  • Thirst.
• With increasing volume depletion, compensation may not be able to maintain MABP.

Clinical correlation: John Doe

• Case: John Doe, motor vehicle accident with trauma - fractured femur, fractured tibia/fibula, +/- multiple lacerations, causing significant blood loss.
• Presentation: pale, cold peripheries, HR 120 bpm, BP 90/50 mmHg (MABP = 63 mmHg) = shock.
• Baroreflexes are operating (increased HR, peripheral vasoconstriction causing cold, pale skin), but the blood losses are significant enough that reflex compensation alone is insufficient.
• Management principles: arrest ongoing bleeding, replace volume (IV), normalise CVS/tissue perfusion, manipulate the determinants of BP (HR/SV/TPR), within the “golden hour.”

Self-test

1. Define shock.
2. Write the equation for MABP in terms of its determinants, and the equation for CO.
3. Where are the baroreceptors located, and what type of stimulus activates them?
4. Describe the four efferent limbs of the baroreceptor reflex triggered by a fall in arterial pressure, and how their effects combine to restore MABP.
5. List the three classes of shock and, for each, state which determinant of MABP is primarily affected.
6. Distinguish anaphylactic, septic and neurogenic shock as subtypes of distributive shock.
7. List the three timescales of the homeostatic response to haemorrhage, with the mechanism operating at each.
8. Describe the steps by which “autotransfusion” restores plasma volume after haemorrhage.
9. Describe the three long-term mechanisms that replace lost volume after haemorrhage.
10. In compensated hypovolaemic shock (<10% loss), describe the blood-pressure compensation response and the volume compensation response.
11. John Doe presents pale and cold, HR 120 bpm, BP 90/50 mmHg after major trauma with significant blood loss. Explain the signs in terms of the reflexes operating, and predict why they may fail to maintain his MABP.
12. Explain why a lecture that separately teaches the baroreceptor reflex and the classification of shock links the two: what happens to MABP when a shock-causing problem is too large for baroreceptor-mediated compensation to overcome?

Answers

Reveal answers

1. Reduced (inadequate) perfusion of tissues with blood, causing decreased delivery of O2 and other nutrients, leading to generalised tissue hypoxia, which if prolonged may cause irreversible cellular damage.
2. $MABP=CO\times TPR$; $CO=HR\times SV$.
3. At the carotid sinus and the aortic arch; they are mechanoreceptors activated by stretch.
4. (1) Decreased parasympathetic discharge to the SA node increases HR. (2) Increased sympathetic discharge to cardiac muscle increases SV. (3) Increased sympathetic discharge to veins causes venoconstriction, raising venous pressure, venous return, end-diastolic volume and so SV further. (4) Increased sympathetic discharge to arterioles causes constriction, raising TPR. HR and SV combine to raise CO; CO and TPR combine to raise arterial pressure back toward normal.
5. Hypovolaemic - decreased volume/preload. Distributive - widespread vasodilation/decreased afterload. Cardiogenic - decreased cardiac output (pump failure or extracardiac obstruction).
6. Anaphylactic - immune reaction releasing histamine, marked peripheral vasodilation, +/- increased capillary permeability, decreased circulating volume. Septic - marked inflammatory response with chemically mediated vasodilation, increased vascular permeability and platelet aggregation. Neurogenic - loss of sympathetic vasomotor tone, from cervical cord injury, decreased central vasomotor control, or anaesthesia.
7. Immediate - baroreceptor reflex. Intermediate - fluid shift from tissues to capillaries (autotransfusion). Long term - replacement of fluid and red cells.
8. The baroreceptor reflex causes arteriolar constriction, which lowers capillary hydrostatic pressure; this increases fluid absorption from the interstitial compartment into the capillaries, increasing plasma volume and helping restore arterial pressure toward normal.
9. ADH release causing water retention; reduced renal perfusion activating the renin-angiotensin-aldosterone system to retain Na+ and water; thirst.
10. Blood pressure compensation: decreased baroreceptor activity activates CNS pressor areas, causing arteriolar vasoconstriction (raising TPR, lowering renal blood flow/urine output), increased HR and contractility (raising CO), and venoconstriction (raising venous return, SV and CO) - all raising MABP toward normal. Volume compensation: arteriolar constriction lowers capillary pressure and drives fluid reabsorption; lower atrial pressure triggers ADH release; lower renal perfusion activates the renin-angiotensin-aldosterone system; thirst is stimulated.
11. His baroreflexes are active: parasympathetic withdrawal drives the tachycardia (HR 120), while sympathetic discharge drives the arteriolar vasoconstriction (cold, pale peripheries) and venoconstriction, together attempting to raise CO and TPR to defend MABP. His BP (90/50, MABP 63 mmHg) is nonetheless low because his blood loss is significant enough that the reflex’s compensatory increases in HR/SV/TPR cannot fully offset the fall in preload and volume - reflex compensation has a limit that severe hypovolaemia can exceed.
12. When the problem causing shock (loss of volume, vasodilation, or pump failure) is too large, the baroreceptor reflex’s adjustments to HR, SV and TPR are not sufficient to bring MABP back to normal, so the fall in MABP becomes persistent - this persistent hypotension despite reflex activity is shock.