Cardiovascular Physiology

1. What this chapter covers, and how NEET PG actually tests it

Cardiovascular physiology is one of the few pre-clinical subjects that NEET PG tests as though it were clinical medicine, because it essentially is.

A question rarely asks what the v wave represents. It describes a patient with a giant v wave and asks what is wrong with the tricuspid valve.

Every waveform in this chapter is a mechanical event made visible, and once you know which event produces which deflection, the abnormal waveform names its own lesion.

The same applies to pressures. A set of haemodynamic numbers from a patient in shock is a physiology question wearing clinical clothing, and it is answered by asking what the heart, the vessels and the filling pressures must each be doing.

This chapter covers four areas: the cardiac action potential and conduction, the cardiac cycle with its waveforms and sounds, cardiac output and its determinants, and blood pressure regulation with shock haemodynamics.

2. The cardiac action potential and conduction

2.1 The ventricular action potential has five phases

The working myocardial action potential differs from a nerve's chiefly by having a plateau, and almost everything distinctive about cardiac behaviour follows from it.

Phase 2 is the phase that matters clinically. The calcium entering here triggers calcium-induced calcium release from the sarcoplasmic reticulum, which is what actually produces contraction.

It also lengthens the action potential to roughly 200 to 300 milliseconds, which is comparable to the duration of contraction itself.

So the refractory period lasts almost as long as the twitch, and the heart cannot be tetanised. A cardiac muscle that could summate contractions would be unable to fill, so this is not an incidental property but a requirement for a pump to work.

2.2 The pacemaker action potential is a different shape

Sinoatrial and atrioventricular nodal cells have no stable resting potential, and no phases 1 or 2.

Their phase 4 drifts spontaneously upward, driven by the funny current, a slow inward sodium current activated by hyperpolarisation.

When the drift reaches threshold, phase 0 is produced by calcium influx, not sodium — which is why nodal upstrokes are slow and why calcium channel blockers slow the heart while having little effect on ventricular conduction.

The rate of phase 4 drift sets the heart rate, and this is precisely where autonomic control acts.

Sympathetic stimulation steepens the drift, so threshold is reached sooner and rate rises. Vagal stimulation flattens it and also hyperpolarises the cell, so rate falls.

The intrinsic rates fall in a hierarchy: sinoatrial node around 60 to 100 per minute, atrioventricular node around 40 to 60, and ventricular Purkinje tissue around 20 to 40.

The fastest pacemaker suppresses the others, which is why an escape rhythm's rate tells you where in the hierarchy the failure occurred.

2.3 Conduction velocity and the atrioventricular delay

Conduction speed varies enormously along the pathway, and the order is worth knowing as a sequence.

Purkinje fibres are fastest, at roughly 4 metres per second, allowing near-simultaneous ventricular activation.

The atrioventricular node is slowest, at roughly 0.05 metres per second.

That slowness is deliberate. It creates the atrioventricular delay that lets the atria finish emptying before the ventricles contract, and it protects the ventricles from conducting every impulse during atrial fibrillation.

3. The cardiac cycle

3.1 The pressure-volume loop, read as a sequence of four events

The left ventricular pressure-volume loop is traversed anticlockwise, and each side of it is one phase of the cycle.

Filling occurs along the bottom, with the mitral valve open, ending at end-diastolic volume of roughly 120 mL.

Isovolumetric contraction is the vertical rise on the right, with both valves shut, ending when ventricular pressure exceeds aortic pressure and the aortic valve opens.

Ejection is the top segment, ending at end-systolic volume of roughly 50 mL.

Isovolumetric relaxation is the vertical fall on the left, ending when the mitral valve opens.

Stroke volume is therefore the loop's width, about 70 mL, and ejection fraction is stroke volume divided by end-diastolic volume, normally 55 to 70%.

The area enclosed by the loop is the stroke work performed by the ventricle, which is why the loop is the cleanest way to see what a valve lesion costs the heart.

3.2 Heart sounds and what splitting means

S1 is closure of the mitral and tricuspid valves at the start of systole. S2 is closure of the aortic and pulmonary valves at its end.

Physiological splitting of S2 occurs on inspiration, because negative intrathoracic pressure increases venous return to the right heart, prolonging right ventricular ejection and delaying P2.

Abnormal splitting is then simply a question of what else is delaying one of the two components.

The word "fixed" is doing the work in the atrial septal defect answer, since the shunt abolishes the normal respiratory variation rather than merely widening the gap.

S3 occurs in early diastole during rapid ventricular filling, and indicates a volume-overloaded or failing ventricle. It can be physiological in children and young adults.

S4 occurs in late diastole as the atrium contracts against a stiff ventricle, as in hypertension or left ventricular hypertrophy.

S4 is impossible in atrial fibrillation, since it requires coordinated atrial contraction — a clean piece of reasoning that questions exploit.

3.3 The jugular venous waveform

The jugular venous pulse is a window onto right atrial pressure, and each deflection is a specific mechanical event.

Cannon a waves deserve their own reasoning. In complete heart block the atria contract at random relative to the ventricles, so occasionally the atrium contracts against a closed tricuspid valve and pressure spikes visibly.

The y descent distinguishes the two great pericardial diagnoses.

In tamponade, filling is impeded throughout diastole, so once the tricuspid opens the ventricle cannot accept blood and the y descent is blunted.

In constrictive pericarditis, early filling is unimpeded until the rigid pericardium is reached, so blood rushes in and abruptly stops — a sharp y descent, and the physiological basis of the square-root sign.

Kussmaul's sign, a paradoxical rise in jugular pressure on inspiration, occurs in constriction rather than tamponade, because the rigid pericardium prevents the right heart accommodating the increased venous return that inspiration delivers.

4. Cardiac output and its determinants

4.1 The basic relationships

Cardiac output is the product of heart rate and stroke volume:

$CO=HR\times SV$

Mean arterial pressure is approximated as diastolic pressure plus a third of the pulse pressure:

$MAP=DBP+\frac{1}{3}(SBP-DBP)$

The weighting toward diastole exists because diastole occupies roughly two-thirds of the cardiac cycle at normal rates. At high rates diastole shortens disproportionately, which is why the approximation degrades in tachycardia.

Stroke volume itself has three determinants — preload, afterload and contractility — and each moves the pressure-volume loop in a characteristic way.

4.2 Preload and the Frank-Starling relationship

Preload is the ventricular volume at the end of diastole, and it reflects venous return.

The Frank-Starling law states that increasing preload increases stroke volume, over the physiological range.

The mechanism is length-tension. Stretching the sarcomere improves the overlap of actin and myosin and increases the sensitivity of troponin C to calcium, so more force is generated for the same calcium transient.

This is the mechanism that matches the two ventricles' outputs automatically. If the right ventricle ejects more, the left receives more, stretches more and ejects more — without any neural signal.

On the loop, increased preload widens it to the right, raising end-diastolic volume and therefore stroke volume.

4.3 Afterload and contractility

Afterload is the resistance the ventricle must overcome to eject, approximated clinically by systemic vascular resistance and aortic pressure.

Raising afterload raises the pressure at which the aortic valve opens, so ejection begins later and ends sooner. End-systolic volume rises and stroke volume falls.

Contractility is the force generated at any given fibre length, and it moves independently of preload.

Increasing contractility empties the ventricle further, so end-systolic volume falls and both stroke volume and ejection fraction rise.

Sympathetic stimulation, digoxin and calcium raise it; beta blockade, acidosis and hypoxia lower it.

A useful check when reading a loop is that preload changes move the right-hand edge, afterload changes move the top, and contractility changes move the left-hand edge.

4.4 Coronary perfusion is a diastolic event

The left ventricular myocardium is compressed by its own contraction, so its own blood supply is squeezed shut during systole.

Left coronary flow therefore occurs almost entirely in diastole.

Two clinical consequences follow directly.

Tachycardia shortens diastole disproportionately and so reduces coronary perfusion time, which is why rate control matters in angina.

And aortic diastolic pressure is the driving pressure for coronary flow, which is why severe aortic regurgitation — which collapses diastolic pressure — can cause angina with entirely normal coronary arteries.

Right ventricular pressures are much lower, so right coronary flow continues in both systole and diastole.

5. Blood pressure regulation and shock

5.1 The baroreceptor reflex

Stretch receptors in the carotid sinus and aortic arch continuously report arterial pressure.

The carotid sinus is innervated by the glossopharyngeal nerve and the aortic arch by the vagus.

A fall in pressure reduces receptor firing, which the medulla reads as a need for more output. Sympathetic outflow rises and vagal tone falls, raising heart rate, contractility and vascular resistance.

The carotid sinus responds to both rises and falls in pressure, while the aortic arch responds mainly to rises — an asymmetry that occasionally appears in questions.

Carotid sinus massage exploits this reflex deliberately, increasing the perceived stretch and thereby increasing vagal tone to slow atrioventricular conduction.

The baroreflex acts within seconds. Longer-term control belongs to the kidney.

5.2 Renin-angiotensin-aldosterone

Renin is released by the juxtaglomerular cells in response to three signals: reduced renal perfusion pressure, reduced sodium delivery sensed at the macula densa, and direct sympathetic beta-1 stimulation.

Renin cleaves angiotensinogen to angiotensin I, which angiotensin converting enzyme converts to angiotensin II, chiefly in the pulmonary vasculature.

Angiotensin II raises pressure by several routes at once: direct vasoconstriction, aldosterone release causing sodium retention, thirst and vasopressin release, and a direct effect on proximal tubular sodium reabsorption.

Its constriction of the efferent arteriole is the detail with the most clinical consequences. By constricting downstream of the glomerulus it preserves filtration pressure when perfusion falls.

This is why an angiotensin converting enzyme inhibitor can precipitate a fall in glomerular filtration in a patient with bilateral renal artery stenosis — the compensation it removes was the only thing sustaining filtration.

5.3 Reading shock from its haemodynamics

Shock types are distinguished by three numbers, and the pattern is fully derivable from the underlying failure.

Reason through it rather than memorising the grid.

Hypovolaemia and cardiogenic shock both give low output with reflex vasoconstriction, and are separated by filling pressure alone — an empty tank versus a failing pump against a full one.

Distributive shock is the one with warm peripheries, because the primary defect is loss of vascular tone, and output rises to compensate.

Neurogenic shock is the exception worth noting within that group: sympathetic outflow is lost, so the patient is hypotensive with bradycardia rather than the tachycardia seen in every other form.

7. Common exam traps

• Assuming pacemaker phase 0 is a sodium current. It is calcium in nodal tissue, which is why calcium channel blockers slow the rate but barely affect ventricular conduction.
• Confusing wide with fixed splitting. Right bundle branch block widens the split but preserves respiratory variation; only a shunt makes it fixed.
• Looking for an S4 in atrial fibrillation. It requires organised atrial contraction and cannot occur.
• Reversing the y descent in tamponade and constriction. Tamponade blunts it, constriction sharpens it.
• Expecting Kussmaul's sign in tamponade. It is characteristic of constriction, where the rigid pericardium cannot accommodate inspiratory venous return.
• Forgetting that left coronary flow is diastolic. This is why tachycardia and low diastolic pressure both cause ischaemia independently of coronary anatomy.
• Treating all shock as vasoconstricted. Distributive shock has high output and low resistance, and neurogenic shock uniquely combines hypotension with bradycardia.
• Assuming an angiotensin converting enzyme inhibitor always protects the kidney. In bilateral renal artery stenosis, efferent constriction is what maintains filtration, and removing it drops the glomerular filtration rate.

Summary

• The ventricular action potential's plateau is a calcium current that both triggers contraction and lengthens the refractory period, so cardiac muscle cannot tetanise.
• Pacemaker cells have no stable resting potential; the funny current drives phase 4 drift and calcium drives phase 0, so rate is set by the slope of that drift.
• Intrinsic rates fall from sinoatrial to atrioventricular to Purkinje, so an escape rhythm's rate localises the level of failure.
• Purkinje conduction is fastest and atrioventricular nodal conduction slowest, the latter deliberately creating the atrioventricular delay.
• The pressure-volume loop's width is stroke volume and its enclosed area is stroke work, with normal ejection fraction 55 to 70%.
• Physiological S2 splitting occurs on inspiration; fixed splitting means an atrial septal defect and paradoxical splitting means delayed A2, as in left bundle branch block or severe aortic stenosis.
• S3 reflects rapid filling into a volume-loaded ventricle; S4 reflects atrial contraction against a stiff one and is impossible in atrial fibrillation.
• Jugular deflections are mechanical events: absent a wave in atrial fibrillation, cannon a waves in complete heart block, giant v wave in tricuspid regurgitation.
• A blunted y descent indicates tamponade and a sharp one constriction, and Kussmaul's sign belongs to constriction.
• Cardiac output is heart rate times stroke volume, and mean arterial pressure weights diastole because diastole occupies most of the cycle.
• Frank-Starling matches the two ventricles automatically through length-tension, without any neural signal.
• On the loop, preload moves the right edge, afterload the top, and contractility the left edge.
• Left coronary perfusion occurs in diastole, so tachycardia and a low aortic diastolic pressure both cause ischaemia independently of the coronary anatomy.
• The baroreflex acts within seconds through carotid sinus and aortic arch afferents in the glossopharyngeal and vagus nerves.
• Angiotensin II constricts the efferent arteriole to preserve filtration, which is why blocking it can drop the glomerular filtration rate in bilateral renal artery stenosis.
• Shock types are separated by output, resistance and filling pressure, with distributive shock uniquely showing high output and low resistance, and neurogenic shock uniquely showing bradycardia.