Cardiovascular Physiology CV

Pacemaker cells generate spontaneous rhythmic activity, while conduction pathways coordinate atrial and ventricular activation. Cardiac action potentials differ among cell types because channel expression and function differ.

Connect pacemaker automaticity → conduction sequence → coordinated contraction.

Conduction abnormalities and arrhythmias can reduce effective filling, ejection or perfusion.

Electrical activation precedes mechanical contraction; an ECG records summed surface electrical activity, not direct contractile force.

Ventricular filling, isovolumetric contraction, ejection and relaxation reflect changing chamber pressures and valve states. Cardiac output equals heart rate multiplied by stroke volume; stroke volume depends importantly on preload, contractility and afterload.

For each phase ask: which pressure is highest, which valves are open, and is volume changing?

Heart failure and valvular disease can be understood by altered pressure-volume relationships and compensatory responses.

A valve opens because of a pressure gradient; it does not actively pull itself open.

Flow is driven by pressure difference and opposed by resistance. Vessel radius has a powerful effect on resistance, making arterioles major controllers of regional flow and systemic vascular resistance.

Use the relationship flow ≈ pressure gradient/resistance, then identify what changed.

Vasoconstriction, vasodilation, shock and hypertension all involve changes in pressure-flow-resistance relationships.

High pressure does not automatically mean high tissue flow; resistance may simultaneously be high.

Capillary exchange depends on permeability and hydrostatic/osmotic forces, while local metabolites and endothelial signals adjust arteriolar tone to tissue need. Lymphatic drainage returns excess filtered fluid and proteins.

Link metabolism → local signal → resistance change → altered flow and exchange.

Oedema may result from raised hydrostatic pressure, reduced plasma oncotic pressure, increased permeability or impaired lymphatic drainage.

Oedema is not explained by one universal mechanism; identify which Starling/lymphatic factor changed.

The heartbeat is initiated by specialized pacemaker cells whose membrane potential drifts spontaneously toward threshold. The sinoatrial node normally sets the rhythm because its spontaneous depolarization is fastest under usual conditions. Excitation spreads through atrial tissue, is delayed through the atrioventricular node, and then travels rapidly through the His-Purkinje system to coordinate ventricular activation.

Cardiac action potentials differ by cell type. Working ventricular myocytes have a prolonged plateau that supports contraction and a long refractory period, reducing the possibility of tetanic contraction. Pacemaker cells use different currents to generate automaticity.

The ECG is a body-surface record of summed electrical activity. It is not a direct recording of contraction or pressure. Electrical events normally precede the corresponding mechanical events.

Teach it back: explain why AV nodal delay is useful and why a long ventricular refractory period protects pump function.

The cardiac cycle can be understood by following atrial pressure, ventricular pressure, arterial pressure, valve position and ventricular volume. During filling, atrioventricular valves are open because atrial pressure exceeds ventricular pressure. Ventricular contraction closes these valves; during isovolumetric contraction all valves are closed, so pressure rises without a change in ventricular volume. When ventricular pressure exceeds arterial pressure, semilunar valves open and ejection begins.

After ejection, ventricular pressure falls. Semilunar valves close when arterial pressure becomes greater than ventricular pressure. Isovolumetric relaxation follows until ventricular pressure drops below atrial pressure and filling begins again. Valves are passive: pressure gradients open and close them.

Stroke volume is end-diastolic volume minus end-systolic volume. Cardiac output equals heart rate times stroke volume. Preload, contractility and afterload influence stroke volume through different mechanisms.

Teach it back: narrate one full cardiac cycle without memorizing valve timing—derive every valve movement from pressure gradients.

Blood flow through a vascular bed is driven by a pressure difference and opposed by resistance. For conceptual analysis, flow is proportional to pressure gradient divided by resistance. Vessel radius has a particularly powerful effect on resistance, so arterioles are major controllers of tissue perfusion and systemic vascular resistance.

Mean arterial pressure is supported by the interaction of cardiac output and systemic vascular resistance. Rapid neural regulation uses baroreceptor reflexes and autonomic changes in heart and vessels. Longer-term regulation strongly depends on renal control of sodium, water and extracellular volume.

Clinical reasoning: high arterial pressure does not automatically mean high flow through every organ. A tissue whose arterioles constrict can receive less flow even while systemic arterial pressure rises.

Teach it back: explain how widespread arteriolar constriction can raise arterial pressure yet reduce perfusion in selected tissues.

Capillaries provide a large exchange surface. Small solutes diffuse according to concentration gradients, while bulk fluid movement depends on hydrostatic and oncotic forces plus capillary permeability. The lymphatic system returns excess filtered fluid and proteins to the circulation.

Oedema can therefore arise through several mechanisms: increased capillary hydrostatic pressure, reduced plasma oncotic pressure, increased capillary permeability, impaired lymphatic drainage or combinations of these. The correct explanation requires identifying which force or pathway changed.

Local metabolic control adjusts resistance so active tissues can receive more blood. Endothelial mediators and tissue metabolites participate in matching perfusion to need.

Teach it back: compare the mechanism of oedema in raised venous pressure with oedema caused by lymphatic obstruction.