Blood pressure and cardiac output

Core relationships

• Preload is best measured as left ventricular end-diastolic volume (set by venous return, Starling's law); afterload is the resistance to ejection.
• In a steady state cardiac output is determined mainly by venous return; the heart pumps out what comes back. Right and left ventricular outputs are equal (100%) over time.
• In heavy exercise output rises mainly through heart rate (sympathetic), with stroke volume helped by the muscle pump and venoconstriction.
• About two-thirds of blood volume sits in the veins; venoconstriction returns this blood to the heart early in a bleed.
• Resistances in parallel add as reciprocals, so a low-resistance branch lowers total resistance a lot. The placenta is such a branch: delivering it removes a low-resistance bed and SVR rises within an hour.

Short-term control: baroreceptors

• Stretch receptors in the carotid sinus (glossopharyngeal) and aortic arch (vagus) respond most to pulsatile pressure and rapid change.
• Higher pressure gives vagal slowing and less sympathetic tone. A fall (mild haemorrhage at 90/60 mmHg) reduces firing: tachycardia, venoconstriction, arteriolar constriction and renin release. This is the first and fastest defence.
• Below a mean pressure of about 60 mmHg baroreceptor firing is already minimal; peripheral chemoreceptors take over, and below about 50 mmHg the CNS ischaemic response gives the most powerful sympathetic vasoconstriction of all, a last-ditch response in massive haemorrhage.
• Baroreceptors reset in chronic hypertension.
• Bezold–Jarisch reflex: an almost empty, vigorously contracting ventricle stimulates ventricular mechanoreceptors (vagal C fibres), causing sudden bradycardia and hypotension. It explains abrupt bradycardia when caval compression under spinal anaesthesia removes preload.

Longer-term control: renin–angiotensin–aldosterone and ADH

• A young hypertensive with high renin suggests renal artery stenosis (fibromuscular dysplasia): the kidney senses low perfusion pressure. After an accident with shock, renin rises from low renal perfusion pressure and sympathetic beta-1 stimulation.
• Angiotensin I is converted to angiotensin II mainly in the lungs (pulmonary capillary ACE).
• Angiotensin II: arteriolar and efferent arteriole constriction, aldosterone release, ADH release, thirst.
• ADH rises with volume loss of about 10% (V1 vasoconstriction, V2 water retention).

Pregnancy

• Cardiac output rises 30–50%, mainly from stroke volume; resting pulse rises 10–20 beats/min.
• SVR falls from 6–8 weeks (relaxin, nitric oxide, progesterone, prostacyclin, low-resistance placenta). Blood pressure is lowest in the second trimester; diastolic falls more.
• Blood volume rises about 45%, yet CVP and wedge pressure stay essentially unchanged because vessels become more compliant. Normal filling pressures do not mean she tolerates large fluid loads.
• Renin, angiotensin II and aldosterone are all raised, but vessels are refractory to angiotensin II. Aldosterone drives retention of about 900 mmol sodium and the plasma volume rise; plasma sodium falls slightly because the osmostat is reset lower.
• Labour: each contraction squeezes 300–500 mL into the circulation. Cardiac output and preload peak just after delivery of the placenta (uterine autotransfusion and relief of caval compression): the danger point for mitral stenosis. Monitoring must continue after the baby is born.
• Postpartum diuresis on days 2–5 is tissue (oedema) fluid returning to the blood and being excreted; the extra circulating volume can push women with heart disease into failure.
• Stenotic valves are tolerated poorly; regurgitant lesions better.
• Supine hypotension: the uterus compresses the IVC. Treat by left lateral tilt or uterine displacement.
• Diastolic pressure is recorded at Korotkoff phase V (disappearance); phase IV only when V is absent, and noted.

Pregnancy disorders of pressure and output

Haemorrhage

• Cold, pale skin is alpha-1 sympathetic constriction; the brain and heart keep their flow. The proximal tubule is the renal segment most damaged by prolonged hypoperfusion (acute tubular necrosis).
• Restoring volume after a 2 L bleed: first transcapillary refill of interstitial fluid (minutes to hours, as capillary hydrostatic pressure falls), then renal salt and water retention (aldosterone, ADH) over 1–3 days, plasma proteins in days, and red cells last (haematocrit normalises in 4–8 weeks).
• Haemoglobin is normal early because whole blood is lost.
• Adequate resuscitation is best shown by a urine output above 0.5 mL/kg/hour, with falling heart rate, warm peripheries and falling lactate.
• Myocardial ischaemia in severe haemorrhage: tachycardia shortens diastole and diastolic pressure is low, so coronary filling falls while demand rises: demand ischaemia with ST depression even with normal coronaries.
• In obstetrics: uterine blood flow at term is about 700 mL/min. Hypervolaemia hides losses of 1,000–1,500 mL; a shock index above about 0.9–1.0 is abnormal.

Types of shock

Remember In pregnancy: output up, resistance down, pressure slightly down, filling pressures unchanged.

Exam trap A normal pulse and blood pressure after PPH do not exclude major blood loss; signs appear late in pregnancy.

Exam trap Tachycardia, not hypotension, is the earliest sign of haemorrhage; systolic pressure falls only in class III.

How FCPS asks about this

• Most potent pressor response in massive haemorrhage: CNS ischaemic response (below about 50 mmHg).
• Cardiac output is mainly determined by: venous return; best index of preload is LV end-diastolic volume.
• Conversion of angiotensin I to II: lungs (pulmonary endothelial ACE).
• Mitral stenosis, highest risk in labour: just after delivery of the placenta.
• CVP and wedge pressure at 36 weeks: essentially unchanged despite 45% more blood volume.
• Blood volume restored after haemorrhage by: transcapillary refill first, then renal salt and water retention.
• Septic shock mechanism: endotoxin-driven vasodilatation with low SVR and high output.