6.1 Cardiovascular and Respiratory Physiology

Why Paper A Tests Systems Physiology

"Physiology of the major body systems relevant to dentistry" is a named Paper A blueprint topic in its own right, separate from "human disease relevant to dentistry". Items test the normal mechanism that the disease or drug then disturbs: why adrenaline raises heart rate but can lower diastolic pressure, why a hypoxic COPD patient depends on hypoxic drive, why a supine patient in late pregnancy becomes hypotensive.

Cardiac Output and Blood Pressure

$\text{Cardiac Output (CO)} = \text{Heart Rate (HR)} \times \text{Stroke Volume (SV)}$

$\text{Mean Arterial Pressure (MAP)} = \text{CO} \times \text{Total Peripheral Resistance (TPR)}$

Mean arterial pressure is estimated clinically as diastolic pressure plus one third of the pulse pressure. Stroke volume is governed by three variables:

• Preload — end-diastolic ventricular filling. The Frank-Starling relationship means that increased filling stretches the myocardium and increases the force of contraction.
• Afterload — the resistance the ventricle must overcome, dominated by systemic vascular resistance.
• Contractility — the intrinsic inotropic state, increased by sympathetic beta-1 stimulation.

The Cardiac Cycle and the Conducting System

The impulse originates in the sinoatrial node, the fastest intrinsic pacemaker at roughly 60 to 100 beats per minute, spreads through the atria, is delayed at the atrioventricular node to allow atrial emptying, and then passes down the bundle of His, the bundle branches and the Purkinje fibres.

Autonomic Control and Adrenergic Receptors

This is the physiology that explains adrenaline in a dental cartridge.

At the doses contained in one or two dental cartridges, beta-2 mediated skeletal muscle vasodilatation can offset alpha-1 vasoconstriction, so systolic pressure and heart rate rise modestly while diastolic pressure may fall slightly. The baroreceptor reflex in the carotid sinus and aortic arch buffers these changes: a rise in pressure increases glossopharyngeal and vagal afferent traffic, producing reflex bradycardia and vasodilatation.

Vasovagal syncope, the commonest emergency in dental practice, is the opposite: emotional or painful stimulus triggers sudden parasympathetic surge and sympathetic withdrawal, causing bradycardia, vasodilatation, cerebral hypoperfusion and collapse. Laying the patient flat with legs raised restores venous return and is definitive.

Respiratory Physiology

• Ventilation is driven by negative intrathoracic pressure generated by diaphragmatic descent and external intercostal contraction. Tidal volume is about 500 mL in an adult, of which roughly 150 mL occupies anatomical dead space.
• Gas exchange occurs by simple diffusion across the alveolar-capillary membrane, governed by Fick's law: flux is proportional to surface area and partial pressure gradient and inversely proportional to membrane thickness. Emphysema destroys surface area; pulmonary oedema increases thickness.
• Oxygen transport: over 98% of oxygen is carried bound to haemoglobin. The oxyhaemoglobin dissociation curve is sigmoid. A right shift — caused by increased carbon dioxide, acidosis, pyrexia and raised 2,3-DPG (the Bohr effect) — offloads oxygen to metabolically active tissue.
• Carbon dioxide transport: about 70% travels as bicarbonate generated by carbonic anhydrase within erythrocytes, 23% bound to haemoglobin as carbamino compounds and 7% dissolved.
• Central chemoreceptors in the medulla respond to cerebrospinal fluid pH driven by arterial carbon dioxide and provide the dominant ventilatory drive in health. Peripheral chemoreceptors in the carotid and aortic bodies respond mainly to hypoxaemia.

Clinical link. In a minority of patients with severe COPD, chronic carbon dioxide retention blunts the central drive and ventilation becomes dependent on hypoxic drive from peripheral chemoreceptors. This is the physiological basis for the target oxygen saturation of 88% to 92% in patients at risk of hypercapnic respiratory failure, rather than the 94% to 98% target used for everyone else.

Physiology That Changes What You Do at the Chair

Paper A asks about physiology in order to test clinical judgement. Three linked ideas carry most of the marks. The first is the baroreceptor reflex: carotid sinus and aortic arch receptors detect a fall in arterial pressure and reduce vagal tone while increasing sympathetic outflow, raising heart rate and peripheral resistance. In vasovagal syncope this reflex is overwhelmed by an abrupt increase in vagal activity, giving the characteristic bradycardia with hypotension — the reason a fainting patient is laid flat with legs raised rather than sat forward, and the reason a patient in anaphylaxis, who is hypovolaemic rather than vagal, must never be sat up.

The second is preload and afterload. Lying a patient with severe left ventricular failure flat increases venous return and can precipitate acute pulmonary oedema, so the orthopnoeic patient is treated sitting upright. The third is oxygen carriage: haemoglobin saturation is near maximal at normal alveolar oxygen tensions, so supplemental oxygen benefits the hypoxic patient but not the normoxic one. This is the physiological basis for the modern rule that oxygen in acute coronary syndrome is titrated to saturation rather than given routinely.